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Neuroscientists spark shelter-seeking response by reactivating memory circuit
Using a sophisticated brain-imaging system, neuroscientists at Johns Hopkins Medicine say they have successfully reactivated a specific memory circuit in mice, causing them to seek out shelter when no shelter is actually present.
The researchers say the study, published Sept. 27 in Nature Neuroscience , advances understanding of how memories are structured in the mammalian brain. The findings could one day point to new ways of slowing down or preventing the memory loss that accompanies Alzheimer’s and other neurodegenerative diseases.
Specifically, the team found that stimulating neurons in two areas of mouse brains — the nucleus accumbens, also known as the brain’s “pleasure center” responsible for relaying dopamine-dependent behaviors, and the dorsal periaqueductal gray (dPAG), responsible for defensive behavior — reactivated a “spatial memory” and caused the mice to seek shelter.
“When we artificially reactivate those memory circuits in the brain, it triggers the mouse to do the same thing it did naturally, even without the fear stimuli that cause them to seek shelter to begin with,” says senior author Hyungbae Kwon, Ph.D., associate professor of neuroscience at the Johns Hopkins University School of Medicine.
The scientists say they aimed to map out which areas of the brain are responsible for navigating one’s surroundings, a high-level cognitive function among mammals, including humans. Thus, these experiments, which tested whether such cognitive brain functions can be replayed randomly, may have applications in understanding how other mammals behave, perceive and sense their environment.
In the new experiments, the researchers first allowed laboratory mice to explore their surroundings in a box with a shelter in the corner. The team placed a series of visual cues, including triangles, circles and stripes in different colors, to help the mice locate the shelter based on nearby landmarks. The mice acclimated to the area for seven minutes, entering and exiting the shelter.
Then, the researchers added a visual or auditory looming signal to spur them to seek shelter — also forming a spatial memory relative to their location and the visual cues.
To selectively tag shelter memory neurons, the researchers used a light-activated gene-expression switching system called Cal-light, which Kwon developed in 2017. Once the scientists identified these neurons in the nucleus accumbens, they switched on expression of the genes associated with them, reactivating the shelter-seeking memory in mice while also activating neurons in the dPAG.
In turn, the mice sought out the area of the box where the shelter had once been, when neither the original threat nor the shelter were present.
To get to this point, the researchers first selectively activated neurons in the nucleus accumbens and then, separately, in the dPAG, to see whether switching on neurons in just one area of the brain would cause this behavior.
“Surprisingly, we found that the mice did not seek out shelter when we activated neurons in the nucleus accumbens alone,” Kwon says. “Whereas switching on neurons in the dPAG caused the mice to react randomly, but did not guide them specifically to the area where they sought shelter before.”
“The Cal-light system allowed us to selectively tag a specific function in the brain, helping us to map out memory on a cellular level,” says Kwon.
Eventually, Kwon says this research could provide a foundation for reactivating or engineering memory circuits in people with Alzheimer’s.
“If we understand the macro-level structure of memory, then we may be able to develop more effective strategies to prevent or slow down neurodegenerative diseases using this method,” he says.
The researchers say they hope to understand brain-wide memory structure by selectively tagging and reactivating neurons with different functions in different areas of the brain that lead to other specific behaviors.
“Understanding how all of these memory circuits work together will help us understand brain function better,” he says.
Other researchers involved in the study are Kanghoon Jung, Sarah Krüssel, Sooyeon Yoo, Benjamin Burke, Nicholas Schappaugh, Youngjin Choi and Seth Blackshaw of Johns Hopkins; Myungmo An of the Max Planck Florida Institute for Neuroscience; and Zirong Gu and Rui M. Costa of the Zuckerman Mind Brain Behavior Institute at Columbia University and the Allen Institute.
Funding for this work was provided by the Max Planck Florida Institute for Neuroscience, a National Alliance for Research on Schizophrenia and Depression Young Investigator Grant and National Institutes of Health Grants R01MH107460, 5U19NS104649, K99 NS119788, DK108230 and DP1MH119428.
Fat Alone Doesn’t Disrupt Brain’s Appetite Neurons
Summary: A new study reveals that a high-fat diet alone does not appear to be responsible for changes in brain neurons that regulate appetite and energy balance. Researchers found no immediate effect on neurons in the hypothalamus of mice fed a high-fat, low-sugar diet, suggesting that other nutrients like sugar may play a more significant role in altering brain function.
The study challenges previous assumptions that fat alone was responsible for disrupting energy homeostasis and increasing the risk of metabolic diseases. Future research will explore how different macronutrients affect brain neurons and appetite regulation.
Key facts: A high-fat diet alone did not affect AgRP neurons in the hypothalamus.
Other nutrients, such as sugar, may have a more profound impact on brain function.
Both male and female mice showed no decrease in neuron connectivity after 48 hours on the diet.
Source: DZD
A high-fat diet can promote overweight and increase the risk of metabolic diseases, such as diabetes. In mice brains, this leads to measurable changes in the region of the hypothalamus.
However, fat alone does not appear to be responsible for this, as reported by a research team from the German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE) and the German Center for Diabetes Research (DZD) in the specialist journal Scientific Reports . POMC neurons inhibit food intake, while AgRP neurons promote it. Credit: Neuroscience News The connections between neurons in the brain are constantly changing. Diet has a significant influence on this. It is now known that a high-fat diet can cause changes in the hypothalamus that disrupt energy homeostasis and can increase the risk of metabolic diseases.
Food intake is predominantly regulated within the brain by two types of neurons: AgRP (Agouti-related peptide) and POMC (proopiomelanocortin) neurons. Both are primarily found in the hypothalamus—or more precisely, in the paraventricular nucleus, a core region of the hypothalamus—and have opposite actions. POMC neurons inhibit food intake, while AgRP neurons promote it.
Fat or Rather Sugar?
Previous research showed that AgRP neuron activity in the paraventricular nucleus decreases in mice that are fed a high-fat diet. This was mostly attributed to the high fat content of the diet given to the animals.
However, the food of the studied mice also contained other nutrients, including sugar. It therefore cannot be said with certainty which macronutrient is responsible for the neuronal changes.
The researchers from DIfE and DZD investigated whether it is primarily fat that causes changes in the brain. They fed male and female mice a high-fat and low-sugar diet for 48 hours.
It was important for the researchers to study both male and female mice, as previous studies had often only used males. As a result, it was unclear whether the two sexes respond differently to a high-fat diet.
Other Nutrients of Greater Significance
The examination of the animal brains produced an unexpected result: An effect of the high-fat diet was not identified. The connectivity of AgRP neurons had not decreased in either female or male mice.
This suggests that it is not dietary fat (alone) that is responsible for the previously observed changes in the hypothalamus. The researchers suspect that other macronutrients, such as sugar, have more profound effects on AgRP neurons.
They now want to conduct further studies to explore the role of individual macronutrients on neuroanatomical and functional changes in the brain. About this appetite and neuroscience research news
Author: Birgit Niesing
Source: DZD
Contact: Birgit Niesing – DZD
Image: The image is credited to Neuroscience News
Original Research: Open access.
“ Acute elevated dietary fat alone is not sufficient to decrease AgRP projections in the paraventricular nucleus of the hypothalamus in mice ” by Selma Yagoub et al. Scientific Reports
Abstract
Acute elevated dietary fat alone is not sufficient to decrease AgRP projections in the paraventricular nucleus of the hypothalamus in mice
Within the brain, the connections between neurons are constantly changing in response to environmental stimuli. A prime environmental regulator of neuronal activity is diet, and previous work has highlighted changes in hypothalamic connections in response to diets high in dietary fat and elevated sucrose.
We sought to determine if the change in hypothalamic neuronal connections was driven primarily by an elevation in dietary fat alone. Analysis was performed in both male and female animals.We measured Agouti-related peptide (AgRP) neuropeptide and Synaptophysin markers in the paraventricular nucleus of the hypothalamus (PVH) in response to an acute 48 h high fat diet challenge.Using two image analysis methods described in previous studies, an effect of a high fat diet on AgRP neuronal projections in the PVH of male or female mice was not identified.These results suggest that it may not be dietary fat alone that is responsible for the previously published alterations in hypothalamic connections.Future work should focus on deciphering the role of individual macronutrients on neuroanatomical and functional changes.Join our Newsletter I agree to have my personal information transferred to AWeber for Neuroscience Newsletter ( more information )Sign up to receive our recent neuroscience headlines and summaries sent to your email once a day, totally free.We hate spam and only use your email to contact you about newsletters. You can cancel your subscription any time.
New method harnesses light to activate neurons in the brain
University of Rochester researchers have demonstrated a noninvasive method using BL-OG, or bioluminescent optogenetics, that harnesses light to activate neurons in the brain. The ability to regulate brain activation could transform invasive procedures such as deep brain stimulation that are used to treat Parkinson’s disease and other neurological conditions.
The advantage of this new technique is that it can create brain activation without the use of an implanted device in the brain to deliver physical light, according to Manuel Gomez-Ramirez, an assistant professor of brain and cognitive sciences and with the University’s Del Monte Institute for Neuroscience, and the senior author of the study, which appears in the journal NeuroImage [insert link when available].
“BL-OG is an ideal method for noninvasively teasing apart neural circuits in the brain,” says Emily Murphy, the first author of the study and manager of the Haptics Lab, led by Gomez-Ramirez. “There are still so many things to learn about the structure and function of distinct brain areas and neuronal cell types that will help us understand how healthy brains function.” How to turn on a light-;without a switch
To turn on light in the brain, researchers need a few tools. The first one is optogenetics, an established research technique that uses light to activate or inactivate cells in the brain. The next tool is bioluminescence, the same chemical reaction that gives a firefly its glow, which provides the light optogenetics needs to work.
Combining these tools creates the material needed for BL-OG. But in order to work, BL-OG still needs something to “turn on” the light. The organic substance luciferin, when combined with bioluminescence, creates light that activates the optogenetics and modulates cellular response in the brain without an incision. Previous work by Gomez-Ramirez has shown that the chemical luciferin is harmless to the body.
The researchers in the Haptics Lab tested this combination. They put BL-OG into a pre-determined brain region in mice. They then injected luciferin through a vein in the animal’s tail to activate the targeted cells in the brain. They found that BL-OG effects occur rapidly in the brain, but that these effects could be controlled by scaling the dosage of the luciferin in the animal. ‘Fine-tuning’ bioluminescent optogenetics
The advantage of this technique is we can create brain activation without a cable. There is less risk for infection and other things to go awry because it is a noninvasive method. If we want to standardize this technique in the lab, and potentially in the clinic, it is critical to map all the important parameters around using it. These latest findings allow us to now work on fine-tuning the desired effects of BL-OG based on need and requirements.” Manuel Gomez-Ramirez, assistant professor of brain and cognitive sciences, University of Rochester Medical Center’s Del Monte Institute for Neuroscience Researchers were also able to track the neuromodulation effects of BL-OG through the bioluminescent activity, another potential feature of this method that could provide insight into how the brain works.
The Alfred P. Sloan Foundation supported this research.
University of Rochester Medical Center
Journal reference:
Murphy, E. F., et al. (2024). Strength of Activation and Temporal Dynamics of BioLuminescent-Optogenetics in Response to Systemic Injections of the Luciferin. NeuroImage . doi.org/10.1016/j.neuroimage.2024.120882 .
Brain rejuvenation breakthrough: How limiting glucose could spark new neuron growth
(© Татьяна Макарова – stock.adobe.com) STANFORD, Calif. — Could the secret to maintaining a youthful, sharp mind be as simple as watching our sugar intake? A new study from Stanford Medicine suggests that glucose plays a surprising role in the aging brain’s ability to produce new neurons.
As we age, our brains become less adept at producing new neurons, a process known as neurogenesis . This decline can have far-reaching consequences, contributing to memory loss, reduced cognitive function, and potentially exacerbating neurodegenerative diseases like Alzheimer’s and Parkinson’s. It also hinders recovery from stroke and other brain injuries. However, this new research, led by Anne Brunet, PhD, professor of genetics, offers hope by shedding light on why neural stem cells – the precursors to new neurons – become less active with age .
Using cutting-edge CRISPR technology, Brunet and her team conducted a comprehensive genetic screen to identify genes that, when inhibited, could reactivate dormant neural stem cells in aged mice. Among the 300 genes they discovered, one stood out: Slc2a4, which codes for the glucose transporter protein GLUT4.
“We first found 300 genes that had this ability— which is a lot,” Brunet explains in a statement. “One in particular caught our attention. It was the gene for the glucose transporter known as the GLUT4 protein, suggesting that elevated glucose levels in and around old neural stem cells could be keeping those cells inactive.”
To validate their findings in living animals, the researchers developed an innovative in vivo screening technique. They injected viruses carrying genetic instructions to knock out specific genes into the subventricular zone of aged mouse brains – an area rich in neural stem cells. After five weeks, they examined the olfactory bulb, where newly generated neurons typically migrate.
The results, published in the journal Nature , were dramatic. Knocking out the Slc2a4 gene led to a more than two-fold increase in new neuron production in the olfactory bulbs of old mice. This boost in neurogenesis was accompanied by an increase in both quiescent and activated neural stem cells in the subventricular zone, indicating that the treatment was stimulating the stem cell population itself. Among the 300 genes researchers discovered, one stood out: Slc2a4, which codes for the glucose transporter protein GLUT4. (© vegefox.com – stock.adobe.com) Further investigation revealed that neural stem cells from older mice take up about twice as much glucose as those from young mice. This increased glucose uptake appears to push the stem cells into a more dormant state. By knocking out Slc2a4 and reducing glucose influx, the aged stem cells became more likely to activate and produce new neurons.
“It’s allowing us to observe three key functions of the neural stem cells. First, we can tell they are proliferating. Second, we can see that they’re migrating to the olfactory bulb, where they’re supposed to be. And third, we can see they are forming new neurons in that site,” explains Tyson Ruetz, PhD, lead author of the study and former post-doctoral scholar in Brunet’s lab, in a media release.
The glucose transporter connection opens up exciting possibilities for future interventions. Brunet described it as “a hopeful finding,” suggesting that it could lead to the development of pharmaceutical or genetic therapies to stimulate new neuron growth in aged or injured brains . Perhaps even more intriguingly, it raises the possibility of simpler behavioral interventions, such as a low-carbohydrate diet, that might adjust the amount of glucose taken up by old neural stem cells.
While this research marks a significant step forward in our understanding of brain aging and regeneration, it’s important to note that the study was conducted in mice. Further research is needed to determine if these findings translate to humans and to explore the long-term effects and potential side-effects of manipulating glucose uptake in neural stem cells .
Nevertheless, this study provides a promising new direction for addressing age-related cognitive decline and potentially treating neurodegenerative diseases. By identifying GLUT4 and other key regulators of neural stem cell aging, scientists now have promising new targets for developing therapies to rejuvenate the aging brain. Paper Summary
Methodology
The researchers used CRISPR-Cas9 gene editing technology to systematically knock out over 20,000 genes in cultured neural stem cells from young and old mice. They then assessed which gene knockouts enhanced the stem cells’ ability to activate and divide. To test the most promising gene candidates in living mouse brains, they developed a novel in vivo screening technique. This involved injecting viruses carrying CRISPR components to knock out specific genes in the subventricular zone of aged mouse brains. Five weeks later, they examined the olfactory bulb to quantify newly generated neurons containing the genetic knockouts. Key Results
The in vitro screen identified over 300 genes that, when inhibited, boosted the activation of aged neural stem cells. The in vivo screen validated 24 of these genes, with Slc2a4 consistently emerging as a top hit. Knocking out Slc2a4 in the brains of old mice increased new neuron production in the olfactory bulb by more than two-fold. It also increased the numbers of both quiescent and activated neural stem cells in the subventricular zone. Further experiments revealed that aged neural stem cells take up about twice as much glucose as young ones and that this elevated glucose uptake appears to promote quiescence. Study Limitations
The study was conducted in mice, so it remains to be seen if the findings will translate to humans. The researchers focused on the subventricular zone, but it’s unclear if similar mechanisms apply to other neurogenic regions like the hippocampus. The long-term effects and potential side effects of Slc2a4 inhibition were not evaluated. Additionally, while the screening approach was powerful, it may have missed some important genes. Discussion & Takeaways
This study provides strong evidence that elevated glucose uptake contributes to the decline in neural stem cell function during aging. By identifying GLUT4 as a key regulator of this process, the researchers have uncovered a promising new target for potential therapies to enhance neurogenesis in aged brains. The fact that brief glucose starvation could activate aged […]
Study hints at ways to generate new neurons in old brains
by Stanford University Medical Center Credit: CC0 Public Domain Most neurons in the human brain last a lifetime, and for good reason. Intricate, long-term information is preserved in the complex structural relationships between their synapses. To lose the neurons would be to lose that critical information—that is, to forget.
Intriguingly, some new neurons are still produced in the adult brain by a population of cells called neural stem cells. As brains age, however, they become less and less adept at making these new neurons, a trend that can have devastating neurological consequences, not just for memory, but also for degenerative brain diseases such as Alzheimer’s and Parkinson’s and for recovery from stroke or other brain injury.
A new Stanford Medicine study, published Oct. 2 in Nature , sheds hopeful new light on how and why neural stem cells, the cells behind the generation of new neurons in the adult brain, become less active as brains age.
The research also suggests some intriguing next steps in addressing old neural stem cell passivity—or even stimulating neurogenesis, the production of new neurons, in younger brains in need of repair—by targeting newly identified pathways that could reactivate the stem cells.
Anne Brunet, Ph.D., professor of genetics, and her team used CRISPR platforms, molecular tools that allow scientists to precisely edit the genetic code of living cells, to conduct a genome-wide search for genes that, when knocked out, increase the activation of neural stem cells in cultured samples from old mice, but not from young ones.
“We first found 300 genes that had this ability— which is a lot,” emphasized Brunet, the Michele and Timothy Barakett Endowed Professor. After narrowing the candidates down to 10, “one in particular caught our attention,” Brunet said. “It was the gene for the glucose transporter known as the GLUT4 protein, suggesting that elevated glucose levels in and around old neural stem cells could be keeping those cells inactive.” Dynamic brains
There are parts of the brain, such as the hippocampus and the olfactory bulb, where many neurons have shorter lives, where they regularly expire and may be replaced by new ones, said Tyson Ruetz, Ph.D., a formal post-doctoral scholar in Brunet’s lab and the lead author of the Nature paper.
“In these more dynamic parts of the brain, at least in young and healthy brains,” he said, “new neurons are constantly being born and the more transient neurons are replaced by new ones.”
Ruetz, now the scientific advisor and co-founder of ReneuBio, developed a way to test the newly identified genetic pathways in vivo, “where the results really count,” Brunet said.
Ruetz took advantage of the distance between the part of the brain where the neural stem cells are activated, the subventricular zone, and the place the new cells proliferate and migrate to, the olfactory bulb, which is many millimeters away in a mouse brain.
By knocking out the glucose transporter genes in the former, waiting several weeks, then counting the number of new neurons in the olfactory bulb, the team demonstrated that knocking out the gene indeed had an activating and proliferative effect on neural stem cells, leading to a significant increase in new neuron production in living mice.
With the top intervention, they observed over two-fold increase in newborn neurons in old mice.
“It’s allowing us to observe three key functions of the neural stem cells,” Ruetz said. “First, we can tell they are proliferating. Second, we can see that they’re migrating to the olfactory bulb , where they’re supposed to be. And third, we can see they are forming new neurons in that site.”
The same technique could also be applied to studies of brain damage, Ruetz said. “Neural stem cells in the subventricular zone are also in the business of repairing brain tissue damage from stroke or traumatic brain injury .” ‘A hopeful finding’
The glucose transporter connection “is a hopeful finding,” Brunet said. For one, it suggests not only the possibility of designing pharmaceutical or genetic therapies to turn on new neuron growth in old or injured brains, but also the possibility of developing simpler behavioral interventions, such as a low carbohydrate diet that might adjust the amount of glucose taken up by old neural stem cells .
The researchers found other provocative pathways worthy of follow-up studies. Genes relating to primary cilia, parts of some brain cells that play a critical role in sensing and processing signals such as growth factors and neurotransmitters, also are associated with neural stem cell activation.
This finding reassured the team that their methodology was effective, partly because unrelated previous work had already discovered associations between cilia organization and neural stem cell function. It is also exciting because the association with the new leads about glucose transmission could point toward alternative avenues of treatment that might engage both pathways, Brunet said.
“There might be interesting crosstalk between the primary cilia—and their ability to influence stem cell quiescence, metabolism and function—and what we found in terms of glucose metabolism,” she said.
“The next step,” Brunet continued, “is to look more closely at what glucose restriction, as opposed to knocking out genes for glucose transport, does in living animals.”
More information: Anne Brunet, CRISPR–Cas9 screens reveal regulators of ageing in neural stem cells, Nature (2024). DOI: 10.1038/s41586-024-07972-2 . www.nature.com/articles/s41586-024-07972-2
Provided by Stanford University Medical Center
Key Brain Cell Mechanism Tied to Sensory Selectivity Discovered
Summary: Neuroscientists have discovered how the CP-AMPA receptor in brain cells influences neuron selectivity in response to sensory stimuli. This receptor type makes neurons less selective, which may help explain certain brain disorders like autism and epilepsy.
By manipulating these receptors in mice, researchers observed changes in visual and spatial processing. These findings could lead to new treatments for conditions tied to misfiring neurons, including intellectual disabilities.
Key Facts : CP-AMPA receptors reduce neuron selectivity, impacting sensory response.
Mutations in related proteins are linked to autism and intellectual disability.
Manipulating these receptors in mice improved neuron selectivity and stability.
Source: Johns Hopkins Medicine
Neuroscientists from Johns Hopkins Medicine say they have determined how a brain cell surface molecule shapes the way certain neurons behave.
The research, published October 2 in Nature , reveals how a molecule, the calcium permeable (CP)-AMPA receptor, suppresses a specific neuron’s ability to pay attention to specific external cues, such as your friend’s earrings, according to the study in genetically-engineered mice. Excitatory neurons from the brains of mice are depicted in green, and PV inhibitory neurons are pictured in magenta. Cells are depicted in the deep hippocampus, which helps navigate space, toward the left side of the image. Toward the right side, cells are depicted in the visual cortex. Credit: David Cheon and Ingie Hong Understanding why some neurons are less “selective” about their response to certain cues may also help researchers study schizophrenia, epilepsy and autism — conditions marked by the faulty processing of external cues and misfirings of neurons in the mammalian brain.
“We’ve discovered that the calcium permeable subtype of AMPA receptors has an added role of suppressing the selectivity of a given neuron,” says Ingie Hong, Ph.D., first author and an instructor in neuroscience at the Johns Hopkins University Medicine.
“Until now, the role of these specific receptors in the wider mammalian brain as it functions in everyday life has been a mystery.”
Along with Hong, the research was led by Richard Huganir, Ph.D., Bloomberg Distinguished Professor of Neuroscience and Psychological and Brain Sciences and director of the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine, who has been studying AMPA receptors for more than 40 years.
AMPA receptors are critical to the fast transfer of information and memory formation in the brain, such as hearing and remembering a person’s name. The subtype of AMPA receptors in this study, CP-AMPA receptors, act as a “gate” that lowers the selectivity of parvalbumin (PV) neurons, which are inhibitory and thereby cast unselective inhibition to nearby neurons, the researchers say.
“Selective neurons will respond to something really specific, for example, your grandfather’s mustache, whereas less selective neurons will respond to different faces or people as well,” Hong says.
“We’ve been looking for the mechanisms and molecules that control this specificity, or selectivity, and how it goes awry in conditions such as autism and epilepsy, where excitatory neurons can become overstimulated.”
The researchers also found that mutations of GluA2, a protein subunit within the CP-AMPA receptor, are associated with intellectual disabilities.
“Human mutations in the GluA2 subunit of the AMPA receptors, which regulates the calcium permeability of the receptor, can lead to intellectual disability and autism,” says senior author Huganir. “This suggests tight control of AMPA receptor calcium permeability is essential for human cognition.”
Specifically, the investigators focused on CP-AMPA receptors in two distinct areas of the brain, the visual cortex, where neurons process visual information, and the hippocampus, where neurons respond to “where you are, where you are headed, or where you have been,” Hong says.
To conduct their research, the scientists developed novel adeno-associated virus vectors to replace calcium permeable AMPA receptors with impermeable counterparts and express them in the mouse brain. They say they hope these vectors can help treat disorders that arise from AMPA receptor mutations in the future.
To map out PV neuron selectivity, the scientists used advanced imaging techniques to observe neuron structure and activity deep within genetically engineered mice brains while showing them video stimuli.
“In most cases, we found that these PV neurons, which are typically less selective, became more selective to visual stimuli as well as spatial location when we swapped out CP-AMPA receptors for impermeable molecules, making inhibitory neurons act more like excitatory neurons,” Hong says.
The researchers say the high amount of CP-AMPA receptors in PV neurons is well-conserved across many species of mammals, including humans.
“Making neuron inhibition less selective makes our neural circuits more efficient than species that don’t have this molecular feature,” Hong says. “It probably also means that our neural networks are more stable.”
Hong says the new research may also have implications for machine learning used in artificial intelligence.
“In machine learning, there are many computerized ‘artificial’ neurons that are trained to be very selective or less selective,” he says. “We’re trying to find how specific and less specific units can work together to give us smarter machines and smarter AI.”
Up next, the scientists intend to study other critical molecules known to change cognition.
In clinical neuroscience, Hong says, a better understanding of which brain molecules contribute to biased neuronal computations in patients could advance the search for drug therapy targets in psychiatric disorders with a genetic component, a budding field Hong calls “neurocomputational therapeutics.”In addition to Hong and Huganir, other scientists who contributed to this study are Juhyun Kim, Dong Won Kim, Richard C. Johnson, Nathachit Limjunyawong, Zhuonan Yang, David Cheon, Taeyoung Hwang, Amit Agarwal, Xinzhong Dong, Seth Blackshaw, Dwight E. Bergles and Solange P. Brown of Johns Hopkins; Thomas Hainmueller, Thibault Cholvin and Marlene Bartos of University of Freiburg; Joram Keijser and Henning Sprekeler of Technical University of Berlin; Soo Hyun Park and David A. Leopold of the National Institute of Mental Health; Fenna M. Krienen of Princeton University; and Steven A. McCarroll of Harvard Medical School. Funding : Funding for this research was provided by National Institutes of Health grants R37NS036715 and U01DA056556. About this sensory neuroscience research news Author: Alexandra Carolan Source: Johns Hopkins Medicine Contact: Alexandra Carolan – Johns Hopkins Medicine Image: The image […]
Neuroplasticity: How New Experiences Impact Your Brain
a close-up of a game board When it comes to defining neuroplasticity, there’s a little quiz that neuroscientist Sandra Bond Chapman, Ph.D ., likes to pose. Think about how much control you have over changing the health of your heart, your brain, and your teeth. What order would you put those in—meaning, which of those do you have the most control over, in terms of improving how well they work?
“If you’re like most people, you’ll say your teeth, heart, and then brain,” says Dr. Chapman, the chief director of the Center for Brain Health at the University of Texas at Dallas. “But it’s actually the opposite: Brain, heart, teeth. The brain is more changeable than our teeth. We care for our teeth several times a day—if we cared for our brain that much, it would be phenomenal.”
And that, says Dr. Chapman, is neuroplasticity . “Neuroplasticity means that our brain’s systems—the neurons and the connections between them—are highly modifiable. And the way they’re modified is by how we use our brain,” she says. “The old thinking was that your brain is fixed and set pretty much after adolescence, and nothing could be further from the truth. Our brain changes moment by moment by everything we think, create, and feel. Neuroplasticity just means it’s changing. And it can change in good ways or bad ways.” The brilliant network
A quick, simplified 101 on the brain: Neurons are nerve cells; electrical signals are sent from neuron to neuron via a vast network of connections between them. It’s those connections that allow us to think and feel emotions. The brain’s network is vast and complicated, made up of 120 billion neurons.
Neuroplasticity is the ability of your brain to make new neural pathways, and change the ones that already exist, in response to changes in your behavior and environment. It’s also what lets the brain rewire itself after the damaging effects of a stroke or other traumatic events that have an impact a person’s abilities.
To envision this, says Dr. Chapman, think about the massive networks involved in air traffic—all the different flying patterns and airports and hubs. “Your brain has different hubs in different flight patterns, different connection patterns,” she says. “Those connections can change and rewire and reconfigure based on how we use it.” When a plane is flying and there’s a storm at one location, it can be rerouted to a different airport—and the brain does that too: “When part of the brain is not working as well, the brain has the capability to work around things and still get places—it just might take a little bit longer.”
Dr. Chapman is the co-leader of the BrainHealth Project at the Center for Brain Health, a scientific study to measure people’s ability to affect their brain fitness. She explains that there are different levels of how the brain specifically changes in response to stimuli. “For instance, how the different neurons communicate with each other—how fast the brain sends signals—can change,” says Dr. Chapman. “You know when you’re having trouble finding a thought or word? Your brain’s speed is a little bit sluggish. Let’s say you haven’t slept well. The speed of connectivity across the different networks works more slowly—and you feel those changes rapidly the next morning.” This is an example, she points out, of neuroplasticity and how quickly the brain can change as a result of our behavior and other stimuli.
Along with the connectivity of the neurons, Dr. Chapman adds, neurochemicals change too. “You’ve got these connections that are wired together, but the signals are sent through chemicals called neurotransmitters, and those change too by how you use your brain. You’re changing the neural chemistry of your brain by how you use it or don’t use it.”
Scientists can measure so much more about the brain than they could even eight years ago, Dr. Chapman says. “In the past, we used to only be able to look at how the structure of the brain changes, and structure changes much more slowly.” Now, science can see how brain function changes as well, she says. “If you’re multitasking and have constant distractions, or are sleep deprived or chronically angry, these are things that can be literally toxic to the connections and the neurotransmitters.” And that’s neuroplasticity too, she points out. Wellness for your mind
Brain science is constantly exploding and evolving, but current research shows various ways neuroplasticity is influenced. Chronic stress, for example, has been shown in studies to have a negative impact. And a healthy diet, regular exercise, and good sleep habits have been shown to have a positive effect.
Dr. Chapman believes that multitasking is a particularly toxic habit when it comes to brain health. “When you’re multitasking, you’re fraying the connectivity,” she says. The brain is designed to focus on one thing at a time, she says, and when you multitask, you’re asking your brain to toggle between two tasks.
Also toxic for the brain is constant distractions—for example, not being able to focus for more than three minutes. “That’s the average time people can attend to a task now, because of how we use technology,” Dr. Chapman says. “In the BrainHealth Project training, we like to get people to focus on a task for at least 20 minutes, or even 45 minutes if they’re doing something that requires innovative thinking.” It’s so hard for people, she adds, because we’ve trained our brains to be distracted. “Because of that, you’re not building strong pathways for your frontal lobe network,” she says.
Another key idea in the BrainHealth Project is what Dr. Chapman calls big idea thinking . “That’s what allows your brain to strengthen those frontal lobe networks and to continuously build a stronger functioning brain,” she says. Taking in too much information makes the brain “kind of a shallow processor. So big idea thinking is when you take in less information and do more with it, go deeper with it and synthesize it. ‘What are the themes? What is the essence? How […]
New Zealand court rules that even lower-level 0.7 mg/L fluoride in drinking water presents “unreasonable risk of injury to health or the environment”
09/30/2024 // Ethan Huff // Views
Tags: badhealth , badpollution , big government , brain damaged , brain function , brain health , clean water , court , Dangerous , Ecology , environment , Fluoridation , Fluoride , Mind , mind body science , New Zealand , poison , progress , rational , tap water , toxic chemicals , toxins , Water Wars A federal court judge in New Zealand has ruled that water fluoridation at a decreased level of 0.7 milligrams per liter (mg/L) of water is still toxic to people and the environment, creating an “unreasonable risk of injury to health or the environment.”
Following a long, drawn-out legal battle, plaintiffs in a case against water fluoridation successfully argued that it simply does not make sense to continue lacing public water supplies with fluoride chemicals.
“Plaintiffs have proven, by a preponderance of the evidence, that water fluoridation at the level of 0.7 mg/L – the prescribed optimal level of fluoridation in the United States – presents an ‘unreasonable risk of injury to health or the environment,'” the judge ruled in the case.
Across New Zealand, most fluoridated water supplies fluoridate at a level of 0.85 mg/L, with some councils fluoridating even higher at the top-end amount of one part per million (1 ppm) of fluoride.
(Related: Did you know that fluoride does absolutely nothing to protect teeth from cavities, despite what public health authorities claim?) Drinking fluoridated water lowers one’s IQ
Drawing from a pool benchmark dose analysis carried out by renowned toxicologist Prof. Philipe Grandjean, who is famous for his work on mercury neurotoxicity, the judge highlighted the fact that drinking fluoridated water causes a child’s IQ to drop.
“The pooled benchmark dose analysis concluded that a 1-point drop in IQ of a child is to be expected for each 0.28 mg/L of fluoride in a pregnant mother’s urine,” the judge explained. “This is highly concerning, because maternal urinary fluoride levels for pregnant mothers in the United States range from 0.8 mg/L at the median and 1.89 mg/L depending upon the degree of exposure.”
“Not only is there an insufficient margin between the hazard level and these exposure levels, for many, the exposure levels exceed the hazard level of 0.28 mg/L.”
Other research confirmed that people who drink fluoridated water show noteworthy levels of fluoride in their urine. In New Zealand’s Palmerston North, which is fully fluoridated, test subjects showed levels of fluoride in their urine at 0/82 mg/L.
Mothers who drink fluoridated water while pregnant were shown to give birth to children with sustained central nervous system damage that likewise results in lowered IQ and symptoms of ADHD, anxiety, and / or depression.
Dr. Diana Sarfati, New Zealand’s Director-General of Health, now has the option to completely call off all water fluoridation efforts across the country in order to protect the nation’s citizens, and especially its children. The question remains: will she do it ?
Fluoride Free New Zealand has created a petition that it is urging people to sign calling for an end to all water fluoridation in New Zealand. Be sure to check it out and sign!
“It’s a good sign, but it needs to go to the top supreme court to be valid and implemented,” tweeted someone on social media in response to the news.
Others here in the United States shared Fluoride Free NZ’s tweet about the court ruling with their own politicians – one this writer saw shared it with Florida Gov. Ron DeSantis for his consideration – so perhaps they, too, will take similar action.
“They’re still poisoning us with the death shots, so they’re not going to stop poisoning our water,” tweeted another with a more skeptical take on the situation.
“All those of us that stood against fluoridation were called all kinds of nasty crap,” added Counterspin Media NZ to the conversation. “It may have been because those that targeted us, were themselves affected by lower IQ?”
More related news about the dangers of fluoride consumption and exposure can be found at Fluoride.news .
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A Scientist Explains How Brains Form Memory—and What Causes Memory Loss
There are so many reasons—normal, non-scary reasons—why we forget things, whether it’s the name of that dog-walking neighbor, or our friend’s birthday, or where we parked our car. Sometimes we’re moving at too fast a pace, multi-tasking all the way. Or maybe our lives are full of too much stress and too little sleep .
Of course, there are more serious and definitely scary-to-consider reasons why people become forgetful—and those are the ones we worry about. The fear is understandable, given the constant flow of news about dementia , as well as our own possible experiences with loved ones.
To understand more about memory , memory lapses, and cognitive dysfunction, here’s a look at how a memory is created in the brain, as well as what’s happening when a person’s recall starts to slip. How a memory is formed
Let’s say you walk in the door and put your keys down next to the coffeepot. “When you do that—when you have any experience—a certain pattern of activity happens in specific neurons (or nerve cells ), and specific neurons are activated,” says neuroscientist Tara Tracy, Ph.D ., assistant professor and a specialist in neurological decline at the Buck Institute . “The strength of those neurons’ activity will affect how well you remember it later. In order to form a memory, there needs to be a strong activation of the neurons, and then there needs to be a plasticity effect—meaning, there needs to be some kind of little change in the brain.” ( Plasticity refers to the brain’s ability to make new neural pathways, and change the ones that already exist, in response to changes in your behavior and environment.)
But maybe when you drop those keys next to the coffeepot, there’s a lot going on in your mind: You’re thinking, I have to gas up the car when I go out again, and whoa, this floor needs washing, and did anyone pick up the dry cleaning? while you’re simultaneously putting away the groceries and glancing at a text. In that case, says Tracy, there’s a good chance that the neurons were only weakly activated. Then, it’s much more likely that you’re going to forget later where you left your keys, she says, “because a weakly activated neuron will not encode the information as well in the brain. There won’t be that plasticity effect when the neurons are only weakly activated.”
This is something that Tracy’s lab at the Buck Institute is focusing on: the “little change in the brain” that allows the memory to encode. “We think this is happening at the synapses , the connections between neurons,” she says. “When the neurons get activated during an experience, synapses within a certain region of the brain will start to strengthen. And that strengthening is what we think encodes the memory.” Lifestyle and memory
How you go about your days and nights can have a definite impact on your memory. For example:
Sleep is seen to be critical to how our brains store memories, though researchers aren’t entirely sure why; those quiet hours seem to give the brain the chance to consolidate memories, as well as to clear toxins and waste products.
Exercise , especially when it’s moderate to vigorous, was found in a large, long-term study to improve memory as well as overall cognition. Exercise helps your brain form more connections between neurons, among other things. The CDC recommends 150 minutes of moderate activity a week—and points out that short bouts of movement add up.
Stress has been shown in multiple studies to affect how our brain stores and retrieves memories. When you’re under high stress the body releases the hormone cortisol, which affects parts of the brain involved in the processing of memory. When cognition declines
“Some loss of cognitive function— age-related cognitive decline —is normal at a certain point,” says Tracy. Everyone experiences it as they get older, to some degree or another.
According to Mayo Clinic , another stage is mild cognitive impairment , in which people may have issues with memory, finding the right words, or impaired judgment, but they usually can go about their usual life. They, or their loved ones, may notice that they’re not able to track conversations or the plot of a film as well as they used to, or they may get disoriented even in places they know well or are more forgetful than they previously were. There’s no single cause for mild cognitive impairment, and it may get better or worse over time.
When it comes to dementia, Alzheimer’s disease is the most common form , accounting for 60-80% of cases, according to the Alzheimer’s Association . Scientists around the world are working to prevent and treat it.
Tracy’s lab at the Buck Institute is studying memory loss from Alzheimer’s disease and frontotemporal dementia. “Everybody experiences normal age-related cognitive decline, not just people with a disease,” she says. “And so the question is, what are the underlying mechanisms of cognitive aging versus Alzheimer’s disease? Are they the same or different?”
There’s overwhelming evidence, Tracy points out, that Alzheimer’s disease is driven by toxicity in the brain caused by a build-up of two proteins, beta-amyloid and tau. “This build up doesn’t necessarily happen in many people who just have age-related cognitive decline,” she says. “That suggests that the mechanisms are different in each.”
There are similarities, however. “Our research is suggesting that in age-related cognitive decline, and especially in Alzheimer’s disease, the neurons can still be activated in the early stages of memory loss, but the synapses can’t encode,” she explains. “There still is neural activity but the synapses can’t encode it. That’s a separate mechanism.”
Alzheimer’s disease is a progressive disease, Tracy points out; people can live with it for five to ten years, sometimes longer. “In the early stages people’s lifestyle can really be affected, but they probably still remember their family members and can do some things—it’s not severe dementia,” she says. “When it gets to the later stages , when it is severe dementia […]
Top 6 Natural Ways to Improve Memory
If you’re relatively young and healthy, improving your memory may not be the health goal you’re currently most focused on. However, memory impairment is an issue that shouldn’t be taken lightly. Considering that memory is tied to many other brain functions and serves as a window into overall cognitive health, it’s never too early to find ways to improve your memory.
Can you actually improve your memory? Research suggests that yes, you most likely can.
For people struggling with remembering things, concentrating, and making decisions, experts’ advice for how to improve memory includes: Learning new information regularly
Eating an anti-inflammatory diet
Exercising often
Getting enough sleep
Potentially trying certain supplements, including nootropics.
Keep Learning New Things
Challenging yourself with new tasks and “breaking out of your comfort zone” are great ways to encourage neuroplasticity, which is the brain’s ability to adapt to new things. Neuroplasticity describes how your brain responds to challenges and experiences by forming new connections, a fantastic way to improve memory. It happens when the brain reorganizes synaptic connections in response to learning and experiences.
It can be easy to get into a monotonous routine as we age, but continuing to develop new skills is essential for keeping the brain sharp and attentive. The best brain-boosting exercises require concentration, full engagement, and a bit of mental effort. Any activity or hobby that requires hand-eye coordination and complex motor skills is also great for the mind.
Ideally, you want to practice exercises you can become increasingly good at over time since progress is rewarding and fun. Some examples include: Learning a new instrument or language
Building things with your hands (You can watch YouTube videos online for help)
Playing chess and other games, either online or in person
Dancing, yoga, and tai chi
Golfing, tennis, bocce, and similar sports
Doing crossword puzzles or playing board games
Eat an Anti-Inflammatory Diet
One important aspect of improving your memory is providing your brain with the fuel to protect against damage (like free radicals and oxidative stress). Eating an anti-inflammatory diet is one of the natural ways to improve memory.
A diet aimed at protecting cognitive function — and potentially even fighting neurodegenerative diseases like dementia and Alzheimer’s disease — should be filled with antioxidants (from colorful fruits and vegetables), quality proteins, and healthy fats. This eating style has been termed the MIND diet, a cross between the Mediterranean diet and DASH diet, created to support heart health. A 2020 study found that the MIND diet may contribute to cognitive resilience in the elderly.
You’ll want to include plenty of “brain foods” that support focus and memory in your diet, such as: Healthy fats, including olive oil, avocado, coconut, nuts like walnuts, egg yolks, ground flaxseed, and flaxseed oil
High-antioxidant foods, such as leafy greens, peppers, onions, citrus fruits, berries, broccoli, dark cocoa, acai, turmeric, and herbs
Cold-water “fatty fish,” such as salmon, tuna, halibut, trout, mackerel, sardines, and herring, which provide omega-3s
Superfoods like wheatgrass, seaweed, and algae
Green tea and coffee in moderation
Wine in moderation (about one glass a day for women, two for men)
Exercise Regularly Regular exercise has been shown in studies to help protect both short-term and long-term memories. It helps your mind stay sharp by: Halting age-related changes in the hippocampus Increasing circulation and oxygen to your brain Boosting neuroplasticity by stimulating growth factors and neuronal connections, including those facilitated by neurotrophins and myokines Managing inflammation and supporting a healthy immune system Reducing the risk for disorders that can contribute to memory loss, such as diabetes and cardiovascular disease Building resiliency against stress Reducing fatigue Releasing endorphins that fight depression Aerobic exercises like brisk walking, swimming, and cycling are among the best options for older adults, including those with injuries or pain. Get Enough Sleep Sleep impacts not only your energy level but also your focus, memory, problem-solving abilities, emotion regulation, and creativity. Researchers have even found that getting enough sleep (avoiding sleep deprivation) plays a role in long-term and short-term memory consolidation, which takes place during the deepest stages of sleep.Adults need between seven to nine hours of sleep per night to feel their best. Some tips for getting better sleep include: Stick to a regular schedule to support your circadian rhythm (your internal clock). Go to bed at the same time every night and get up at the same time each morning. Limit screen time at night and avoid scrolling through distressing news online. Instead, do something relaxing, such as reading, meditating, or writing. Blue light emitted by electronics, such as TVs, tablets, phones, and computers, can affect your sleep. Try soothing activities, such as listening to music, meditation, or yoga, which can improve cognitive abilities, including focus, creativity, memory, and learning. One study found that meditation and music significantly enhanced subjective memory function and objective cognitive performance in adults with cognitive decline. Avoid alcohol, caffeine, sugar, and spicy foods before bedtime. Take a nap, especially after learning new information. According to some studies, this may help with remembering things more easily. Prioritize Relationships to Fight Loneliness Studies show that meaningful relationships in one’s life and a supportive social circle can help defend the brain against damage since these decrease loneliness, a form of psychological stress.To boost your mood and brain function, make an effort to maintain relationships and reach out to others often. Try finding a community you can actively engage in, such as a church or faith group, fitness centre, sports team, volunteer organization, etc.Laughing with others and physical affection can help release “happy hormones,” such as oxytocin, that can aid in cognitive health. Intentionally seek out and spend time with positive people. Playing with children and pets is another great stress-reducer that can make life more playful and help you take things less seriously.Here’s a tip: If you find it difficult to keep up with an active social life and remember events, try staying organized with the help of calendars, planners, maps, shopping lists, file folders, and address books. These types of things are […]
Fiber photometry technique finds serotonin levels in brain increase with reward value
Ball-and-stick model of the serotonin molecule. Credit: Public Domain Serotonin is often referred to as the “happiness molecule.” It plays a critical role in affecting mood levels and is also a neurotransmitter that sends signals within the brain and the body.
Researchers have generally thought that the chemical plays a global role in modulating brain states by acting over a longer timescale than dopamine, which signals reward but operates on a much shorter timeframe.
Now, a Dartmouth study published in The Journal of Neuroscience reports that serotonin increases in anticipation of a reward and scales with the value of that reward.
For decades, prior research has looked at the release of dopamine levels in encoding the value of rewards at a subsecond timescale using a technique that enabled scientists to monitor it throughout different areas in the mouse brain .
Techniques for monitoring serotonin at this timescale did not previously exist, leaving many unknowns about when serotonin is released in the brain because of its widespread projections. Serotonin is an extraordinarily complex system, with the cells located in one small region of the brain, which then send their messages to pretty much every other area of the brain.
There are 14 serotonin receptors, which are like 14 different locks and the key, serotonin, can fit into any one of those locks, unlocking a different message depending on the door. This explains why past studies have focused on targeting those receptors before it was possible to examine serotonin itself.
“In this research we used a new biosensor called GRAB-serotonin, for short, that could, for the first time, measure the molecule by ‘grabbing’ serotonin released in the brain, while the mouse was running around receiving a tasty treat,” says senior author Kate Nautiyal, an assistant professor of psychological and brain sciences at Dartmouth.
Using a technique called fiber photometry, light can be used to trigger and then measure fluorescence fluctuations from a biosensor like GRAB, whenever serotonin is detected. The team was able to study the release of serotonin in mice while they received rewards, which in this case were varied concentrations of evaporated milk, which mice love. The researchers were then able to look at how serotonin levels changed depending on how good the reward was.
“We had a pretty good understanding that if you alter serotonin signaling by targeting receptors or manipulating reuptake such as with selective serotonin reuptake inhibitors, which are used in antidepressants, you get these broad impacts on mood and can change the way that animals or individuals seem to regulate behavior,” says co-author Mitchell Spring, a postdoctoral researcher who worked on this project in the Nautiyal Lab, a behavioral neuroscience lab in the Department of Psychological and Brain Sciences at Dartmouth.
The results showed that consumption of higher concentrations of the reward was associated with greater serotonin release. When the mice were thirsty and were given water, there was a big serotonin signal, and when they were satiated with a good reward and were full, the serotonin signal was not as strong.
The findings also showed that if you give mice a cue that predicts the reward, serotonin levels rise during the cue, or anticipation, of the reward.
“We found that you can modulate the serotonin signal with the subjective value of the reward,” says Nautiyal. “Our results tell us that serotonin is really a signal in the brain monitoring how good a reward is.”
In measuring the release of serotonin, the team focused on one brain region, the dorsomedial striatum, which has previously been associated very strongly with dopamine, decision-making, and impulsivity.
The researchers say that selective serotonin reuptake inhibitors are widely prescribed and generally effective but we don’t fully understand how they work or what serotonin is doing to address the behaviors that these antidepressants are treating.
“A better understanding of how serotonin is operating at baseline or in healthy individuals during a positive experience could be used to develop more targeted treatments for psychiatric disorders like depression and addiction,” says Nautiyal.
More information: Mitchell G. Spring et al, Striatal serotonin release signals reward value, The Journal of Neuroscience (2024). DOI: 10.1523/JNEUROSCI.0602-24.2024
Citation : Fiber photometry technique finds serotonin levels in brain increase with reward value (2024, September 27) retrieved 28 September 2024 from https://medicalxpress.com/news/2024-09-fiber-photometry-technique-serotonin-brain.html
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Melatonin Making You Groggy? A Better Natural Sleep Aid Might Be GABA
Kiss melatonin’s bleary mornings and overactive dreams goodbye with another natural, silly-sounding sleep aid. You’re tossing and turning all night, and waking up feeling groggy. Maybe you’ve already tried using a new pillow with better neck support but still found it impossible to get a good night’s sleep. Maybe melatonin isn’t working for you either. Many Americans deal with insomnia , and the effects can be serious. Not only can lack of sleep affect your mood ; it can also impair brain function and even weaken your immune system .
The possible causes — and remedies — for this inability to rest can seem endless, but before you take drastic measures, adding a sleep aid supplement to your nightly routine is an inexpensive and often effective treatment. If typical solutions like yoga , journaling or melatonin haven’t worked, consider giving this alternative supplement a try.
Enter gamma-aminobutyric acid or GABA. It’s an amino acid naturally found in the body that promotes a calming effect. GABA is often taken as a dietary supplement, but it has a track record showing that it may be a good sleep aid alternative to melatonin. It affects only the early sleep stages and leaves you feeling more awake in the morning as a result (some people say popular sleep supplements like melatonin make them groggy ). Although there’s limited research, small studies have yielded positive results showing that GABA may be worth a shot if you’re struggling to fall asleep .
Here’s what we know about GABA, tips on taking it and why it might be a viable sleep aid to consider.
For more help getting quality rest, try these seven natural sleep aids for insomnia and how to create the perfect environment for sleep .
Best Mattress of 2024 What is GABA?
GABA is a neurotransmitter naturally found in the brain and some foods like tomatoes and soybeans. It’s an inhibitory neurotransmitter that blocks chemical signals in the central nervous system and reduces brain activity. GABA can help promote calmness in the body and helps regulate nerve cell hyperactivity when feeling fearful, anxious or stressed.
It’s sold without a prescription as a dietary supplement, but GABA’s effects may also benefit those who struggle to fall asleep. Taking GABA for sleep
Taken alone or with other natural sleep aids, GABA supplements help address anxiety, stress and an overactive brain , three main offenders that make it difficult to fall asleep. Its calming effect puts the mind in a relaxed state, so you’re in the right headspace to drift off to sleep.
Low GABA levels have actually been linked to sleep deprivation, as one study found participants with insomnia had 30% lower levels of GABA in their systems. Another small-scale study by Frontiers in Neuroscience involving middle-aged adults found that taking 300 mg of GABA before bed for at least a week can reduce sleep latency (the amount of time it takes to fall asleep).
There’s no concrete evidence showing GABA helps sleep efficiency (quality of sleep and slow wave sleep), but the study’s results showed it may promote sleepiness as it affects early sleep stages. Another benefit is that it won’t leave you feeling drowsy the following morning like other over-the-counter medications such as ZzzQuil or prescription sleep medications. A rendering of the molecular structure of GABA. Artystarty/Getty Images Tips for taking GABA to aid sleep
1. GABA can be taken as a supplement or powder in your food .
2. Take GABA 30 to 60 minutes before bed for the best results (as shown by studies).
3. Follow the dosage instructions and track the amount and how often you take GABA.
4. Use a sleep journal to document your sleep quality so you can identify patterns and possible side effects while tracking GABA’s effectiveness.
5. GABA is naturally found in fermented foods like kimchi, sourdough, sake and mulberry beer.
6 . Always talk to your doctor before taking GABA or any new supplements. Is it safe to take GABA every night?
According to the Sleep Foundation, there are no serious side effects when taking GABA in small doses from sleep or dietary supplements, although some consumers have reported feeling abdominal pain or headaches. High levels of GABA in the brain are linked to daytime drowsiness, and a small number of people report drowsiness after taking GABA.
People at a higher risk of having a negative reaction to GABA include: Pregnant people
People under 18 years old
Those who take prescriptions for high blood pressure
Those who take anti-seizure medications
Other benefits of GABA: stress and anxiety relief
While research is still limited, more data supporting GABA as a stress and anxiety reliever continues to emerge. Relieving anxiety and stress before bed isn’t to be taken lightly, as it can significantly impact sleep latency and overall sleep quality . One study from 2012 showed that after 30 minutes of taking GABA, it helped ease stress in participants.
Low levels of GABA can result in anxiety and depression and are prevalent in individuals with mental health conditions .
There’s a high dose of GABA in the supplement Chlorella as the neurotransmitter has been shown to lower blood pressure. As you should with any new supplement, consult your doctor before taking GABA, especially when taken in combination with other medications or prescriptions.
Grape flavonoids are key to longevity and overall wellness
Tags: #nutrition , aging , brain health , cancer , cardiovascular health , cognitive function , flavonoids , food cures , food is medicine , goodcancer , goodfood , goodhealth , goodmedicine , grape flavonoids , grapes , heart health , longevity , oxidative stress , prevent cancer , resveratrol , superfood , superfoods For centuries, grapes have been a staple in human diets – from ancient civilizations to the vineyards of modern Europe. While they have long been associated with health and vitality, it is only recently that science has begun to unlock their true potential. The secret to their health benefits lies in powerful phytocompound polyphenols called flavonoids , which not only protect the brain and heart but also support overall wellness.
Flavonoids are a group of natural compounds found in plants, including grapes – the most mentioned plant in the Bible scriptures. These powerful antioxidants protect the body from oxidative stress, which plays a significant role in aging and the development of chronic diseases – long-lasting health conditions. Grapes, particularly their skins and seeds, are packed with these potent phytocompounds and they offer a range of benefits for the brain, heart, skin and more. Longevity
The health benefits of flavonoids largely come down to their ability to combat oxidative stress – a process that accelerates aging and damage. Over time, oxidative stress leads to chronic conditions, like cancer, diabetes, heart disease and neurodegenerative diseases – disorders that affect the brain and nervous system like Alzheimer’s or Parkinson’s. Grape flavonoids help neutralize harmful free radicals – slowing the damage caused, extending the lifespan of cells and possibly even extending life expectancy . Heart health and cardiovascular function
One of the most well-known health benefits of grapes and grape-based products, such as red wine, is their ability to support heart health . This phenomenon, known as the “French Paradox” highlights how populations in France, despite consuming diets rich in fats, have lower rates of heart disease. Researchers believe that regular consumption of red wine, which is rich in resveratrol and other grape flavonoids, plays a significant role in this.
Grapes promote heart health and cardiovascular function by the following mechanisms, among many others: Lower blood pressure . Resveratrol helps relax blood vessels, making it easier for blood to flow and reducing strain on the heart.
Improve cholesterol levels . Grape flavonoids help reduce bad cholesterol (LDL) and increase good cholesterol (HDL), lowering heart disease risk.
Prevent blood clots . Resveratrol has been linked to a lower risk of irritation and swelling (called inflammation) and blood clotting properties, which may help reduce the risk of strokes and other cardiovascular events. By lowering inflammation in blood vessels, flavonoids reduce the risk of atherosclerosis – a condition where arteries become clogged with fatty deposits.
Including grapes, grape juice or even moderate wine in diets could support long-term heart and cardiovascular health. Brain health and cognitive function
In addition to protecting the heart, grape flavonoids play a role in preserving brain health. Resveratrol, in particular, has been shown to have neuroprotective properties – helping to protect neurons and prevent the onset of neurodegenerative diseases.
Several studies have demonstrated that flavonoids, the most abundant biologically active phytonutrients among grape polyphenols, improve blood flow to the brain – protecting against cognitive decline (more frequent confusion and worsening memory loss) as we age.
A study published in the Journal of Neuroscience found that flavonoids prevented the formation of beta amyloid plaques – abnormal protein clumps that accumulate in the brains of people with Alzheimer’s – and resveratrol, in particular, improved memory with reduced formation of these harmful unusual clumps and neurofibrillary tangles. This finding provides hope for future therapies aimed at preventing or slowing cognitive impairment in humans. Anticancer
Grape flavonoids have also been studied for their anti-cancer properties. They may help prevent the development of certain types of cancers by inducing apoptosis (programmed cell death) in cancer cells and inhibiting tumor growth.
Research shows that flavonoids such as quercetin and resveratrol can interfere with the growth of cancer cells in the breast, colon and prostate. They may also reduce the risk of metastasis – where cancer spreads from one part of the body to another. Skin health and rejuvenation
Beyond their internal benefits, grape flavonoids also have significant effects on skin health. By protecting skin cells from oxidative damage and UV radiation, these natural compounds help prevent premature aging. They also support the production of collagen – a protein that keeps skin firm and elastic.
The anti-inflammatory properties of grape flavonoids help reduce skin inflammation, which can greatly contribute to conditions like acne (a skin condition that causes blocked pores and pimples), eczema ( a condition that makes skin dry, itchy and red) and rosacea ( a chronic skin condition that causes redness and visible blood vessels).
Embrace grapes as part of a healthy, moderate diet to unlock their full potential for a longer, healthier life.
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Grapes are God’s amazing natural medicine. Watch this video .
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Grapes: Versatile fruit with health benefits .
Facts about grapes and their amazing benefits are proven .
Grapes have long been hailed as the “food of the gods”… they contain antioxidants that protect your health .
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Reversible Brain Mechanism Explains Memory Loss from Drug Abuse
Summary: Scientists have uncovered a mechanism in the brain that explains how drugs like methamphetamine and PCP impair cognitive functions, particularly memory. The study shows that these drugs trigger neurotransmitter switching in the cerebral cortex, where excitatory glutamate neurons switch to inhibitory GABA neurons, leading to memory deficits.
Interestingly, researchers were able to reverse this switch and restore memory performance in mice using molecular tools and the antipsychotic drug clozapine. This discovery could pave the way for developing therapies to counteract drug-induced cognitive impairments and other brain disorders.
Key Facts : Meth and PCP cause neurons to switch from glutamate to GABA, impairing memory.
Reversing this neurotransmitter switch restores cognitive function in mice.
The findings could lead to new therapies for drug abuse and other brain disorders.
Source: UCSD
The effects of sustained drug abuse can manifest in many ways. Loss of memory and reduced cognitive functions are some of the effects that can persist for years. Neurobiologists at the University of California San Diego have now identified a mechanism in the brain that generates drug-induced cognitive impairments.
Scientists in the Department of Neurobiology, School of Biological Sciences, investigated how methamphetamine and phencyclidine (PCP or “angel dust”), which take effect by activating different targets in the brain, induce a similar reduction in cognitive ability. How could the same difficulties in memory emerge in response to drugs that trigger different actions in the brain? “This study reveals a shared and reversible mechanism that regulates the appearance of cognitive deficits upon exposure to different drugs,” said Spitzer. Credit: Neurosicence News The results of this investigation, led by Assistant Project Scientist Marta Pratelli in Professor Nicholas Spitzer’s laboratory, are published in Nature Communications. They showed that meth and PCP caused neurons to change the way they communicate through a process known as neurotransmitter switching.
Neurotransmitter switching is a form of brain plasticity, an evolving area of research investigating how the brain changes function and structure in response to experience. In recent years, Spitzer and his colleagues have also identified roles for neurotransmitter switching in autism spectrum disorder, post-traumatic stress disorder and in exercise.
Examining the cerebral cortex of mice, the investigators found that meth and PCP each caused a switch from the excitatory neurotransmitter glutamate to the inhibitory neurotransmitter GABA (gamma-aminobutyric acid) in the same neurons in the prelimbic region, an area of the frontal cortex involved in executive functions.
This switch was linked to a decrease in memory task performance since drug-treated mice performed well in the tasks when the expression of GABA was blocked.
Further experiments showed that even after repeated exposure to the drugs, the researchers were able to reverse this neurotransmitter switch using molecular tools to locally decrease the brain’s electrical activity or using clozapine, an antipsychotic drug. Each of these treatments reversed the memory loss, restoring the performance of mice in the cognitive tasks.
“These results suggest that targeted manipulation of neuronal activity may be used to ameliorate some of the negative effects of repeated drug abuse,” said Pratelli.
In this new study, the researchers found that a drug-induced increase in the release of dopamine, a neurotransmitter involved in reward, and an increase in the electrical activity of neurons in the cerebral cortex, were required to produce the neurotransmitter switch.
“This study reveals a shared and reversible mechanism that regulates the appearance of cognitive deficits upon exposure to different drugs,” said Spitzer.
The researchers note in their paper that a deeper understanding of brain mechanisms tied to loss of memory from drug use could boost prospects for new treatments, not only resulting in therapy for meth and PCP consumption, but for other disorders as well.
The researchers included Marta Pratelli, Anna Hakimi, Arth Thaker, Hyeonseok Jang, Hui-quan Li, Swetha Godavarthi, Byung Kook Lim and Nicholas Spitzer.
Funding: Funding for the study was provided by the National Institute on Drug Abuse (R21 CEBRA grant DA048633; and R21 DA050821) and the Overland Foundation. About this addiction and cognition research news
Author: Mario Aguilera
Source: UCSD
Contact: Mario Aguilera – UCSD
Image: The image is credited to Neuroscience News
Original Research: Open access.
“ Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits ” by Marta Pratelli et al. Nature Communications
Abstract
Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits
Cognitive deficits are long-lasting consequences of drug use, yet the convergent mechanism by which classes of drugs with different pharmacological properties cause similar deficits is unclear.
We find that both phencyclidine and methamphetamine, despite differing in their targets in the brain, cause the same glutamatergic neurons in the medial prefrontal cortex of male mice to gain a GABAergic phenotype and decrease expression of their glutamatergic phenotype.Suppressing drug-induced gain of GABA with RNA-interference prevents appearance of memory deficits. Stimulation of dopaminergic neurons in the ventral tegmental area is necessary and sufficient to produce this gain of GABA.Drug-induced prefrontal hyperactivity drives this change in transmitter identity. Returning prefrontal activity to baseline, chemogenetically or with clozapine, reverses the change in transmitter phenotype and rescues the associated memory deficits.This work reveals a shared and reversible mechanism that regulates the appearance of cognitive deficits upon exposure to different drugs.Join our Newsletter I agree to have my personal information transferred to AWeber for Neuroscience Newsletter ( more information )Sign up to receive our recent neuroscience headlines and summaries sent to your email once a day, totally free.We hate spam and only use your email to contact you about newsletters. You can cancel your subscription any time.
Biblical superfoods: Ancient healing foods are also useful in modern times
Tags: ancient wisdom , Bible food , bitter herbs , flaxseed , food science , functional food , goat milk , goodfood , goodhealth , goodmedicine , grapes , grocery cures , gut health , health science , honey , longevity , natural cures , natural health , natural medicine , olive oil , Olives , organics , phytonutrients , raw milk , superfoods , timeless wisdom Ancient scriptures and spiritual teachings, including the Bible, offer profound insights into how we should live and what we should eat. People in the Bible were even said to live beyond 900 years – with Methuselah, the longest-lived person in the Bible , dying at the age of 969.
The Bible emphasizes that we should treat our bodies with care and respect, viewing them as spiritual vessels . Throughout its teachings, four key concepts emerge: cleanliness, good nutrition, fasting and exercise.
What’s even more fascinating is that many of the foods mentioned in the Bible aren’t just symbols of faith, but are now recognized as superfoods for their healing and therapeutic properties in modern research. Could it be that we’ve had timeless dietary advice at our fingertips all along?
Let’s dive into the Bible’s dietary recommendations and compare them to what we know about healthy eating today. You might be surprised to find that ancient wisdom and modern science agree on the health-supporting power of these biblical superfoods.Bitter herbs: Nature’s digestive aid
(Exodus 12:8)
In the Bible, bitter herbs like maror are mentioned during the Passover Seder meal. While their bitterness might make them a challenge for some, it is worth developing a taste for them. These herbs are packed with compounds that aid digestion and support liver function . Modern research shows they can also reduce inflammation and even help regulate blood sugar levels. So, don’t shy away from bitter greens, like arugula or dandelion – they’re like a natural boost for your gut and overall well-being. (Related: Use bitter herbs for optimal digestion and detoxification .)Fish: Brain food from the seas
(John 21:11-13; Matthew 15:36)
Fish, especially cold-water varieties like cod or salmon, is hailed as one of the healthiest foods on the planet. The Bible frequently refers to fish as a staple – and for good reason. Packed with high-quality protein and omega-3 fatty acids, fish reduces inflammation and supports cognitive function. It is also rich in iodine, which is crucial for thyroid health and metabolism. Modern research shows that people who eat more fish tend to experience slower mental decline as they age. So, when you enjoy fish, you’re feeding both your body and brain!Flaxseed: The tiny superfood
(Proverbs 31)
Flaxseed might be small but they pack a punch – delivering significant health benefits as indicated in a study published in Healthcare . Known in ancient times as a source of nourishment, flaxseed is rich in fiber and omega-3 fatty acids – reducing inflammation, improving digestion and supporting heart health. Today, flaxseed is celebrated for their ability to lower blood pressure, regulate blood sugar and even combat free radicals in the body. Just be cautious and don’t overdo it – too many can have a powerful laxative effect and might result in an overly active digestive system!Grapes: The anti-aging superfruit
(Deuteronomy 23:24; Leviticus 19:10)
Grapes are perhaps the ultimate anti-aging food mentioned in the Bible. They are rich in resveratrol, an antioxidant found in grape skins, which has been linked to longevity. Resveratrol helps activate the “longevity gene,” sirtuin, which plays a key role in cellular repair and regeneration, as indicated in a study published in the Journal of Clinical and Experimental Cardiology. This compound is also being researched as a potential treatment for age-related diseases, like osteoporosis. Even wine, made from grapes, carries some health benefits when enjoyed in moderation. Pairing grapes with other anti-aging foods, like broccoli, cabbage and cucumbers, which boost nicotinamide adenine dinucleotide (NAD+ ) levels in the body, could be your recipe for long-lasting vitality.Honey: Nature’s sweet medicine
(Deuteronomy 8:8; Exodus 33:3; Genesis 43:11; Judges 14:8-9)
Honey, often seen as a symbol of abundance in the Bible, is far more than just a sweet treat – it’s a natural sweetener that never spoils. In biblical times, honey was a prized commodity, particularly because processed sugar didn’t exist. All honey consumed then was local and raw, ensuring its high quality and potency. The honey of that era would have been quite different from what we commonly find today. Local honey is especially beneficial for people with allergies. Since bees collect nectar from flowers in the local environment, consuming honey from nearby hives introduces small amounts of allergens into the body. Over time, this can help the body build a natural defense, reducing allergic reactions when exposed to the same allergens in the future. (Related: Honey: The ultimate survival food that doesn’t expire .)
In ancient times, honey was valued not only as a natural sweetener and energy source but also for its nourishing and healing properties. Packed with antioxidants, honey boosts the immune system , acts as a natural antibacterial, aids digestion and helps manage blood sugar levels. Today, we recognize honey as a much healthier alternative to processed sugar – making it as valuable now as it was in biblical times. Milk: Nourishment for body and bones
(Exodus 33:3; Job 10:10; Judges 5:25)
When the Bible speaks of a “land flowing with milk and honey,” it references two of the most nourishing food staples of the time. In biblical times, people drank raw milk, which is rich in beneficial enzymes, probiotics and nutrients. Raw milk, particularly from goats (and sheep), is easier to digest . Today, modern milk undergoes pasteurization, which removes many of these beneficial components. Research shows that after heat treatment, pasteurized milk has less copper, iron and manganese.
Raw milk is making a comeback for its health benefits. Goat milk (which is also mentioned in the Bible in Proverbs 27:26-27 King James Version) is easier to digest, especially for those with lactose intolerance – making it […]
STUDY: Food dye tartrazine temporarily makes skin and muscle TRANSPARENT
09/24/2024 // Olivia Cook // Views
Tags: breakthrough , chemicals , Chemistry , discoveries , food coloring , food dye , food science , future science , goodfood , goodhealth , goodmedicine , goodscience , health science , ingredients , medical diagnostics , medical imaging , physics , research , tartrazine A new study has found that tartrazine, a food dye commonly known as “FD&C Yellow 5,” can temporarily make muscle and skin transparent . Researchers now believe this unique phenomenon can one day be used in medical diagnostics to help diagnose illnesses .
By applying this dye to live mice, scientists have been able to observe internal organs, like blood vessels, intestines and the liver. Once the dye is washed off, the skin’s normal appearance returns. The team at Stanford University that made his discovery has yet to test the effect of tartrazine on humans, but they believe that if it is effective, it could revolutionize medical diagnostics. (Related: STUDY: Voice analysis tech can accurately detect Type 2 diabetes through speech patterns .)
Guosong Hong, a leading researcher on the project and an assistant professor of materials science and engineering at Stanford, explained that this method could eventually allow doctors to diagnose internal tumors without resorting to costly and invasive biopsies. This technique might also make blood draws less painful by helping medical professionals quickly and accurately find veins.
When light hits the skin, it normally scatters – making the skin appear solid and opaque. This happens because different parts of the tissue, like fat and water, bend light in different ways – a property known as the refractive index. This is the same phenomenon that makes a pencil look bent when placed in water.
Tatrazine changes how light passes through the skin by matching these refractive indices, particularly at certain wavelengths of light, which reduces scattering and makes the skin appear transparent.
Lead researcher Zihao Ou of Stanford’s Wu Tsai Neurosciences Institute and his colleagues proposed that certain types of dyes could make these tissues more transparent by absorbing specific wavelengths of light. The dyes work by altering the refractive index of the tissues, enabling the researchers to match the refractive indices across different tissue types and reduce light scattering.
In the study published in the journal Science , the research team showcases how a fresh chicken breast became transparent to red light shortly after being immersed in a solution containing tartrazine. The dye worked by minimizing light scattering within the tissue – allowing the light to pass through more effectively.
With this method on live mice, the researchers were able to see the functioning of several internal organs in real time. They observed the intestines, liver and even the beating heart of a live mouse – all without the need for any special equipment.
The transparency also allowed them to see blood flow in the brain and the fine details of muscle fibers. More importantly, the dye did not cause any permanent changes to the skin and the effect disappeared as soon as the dye was rinsed away with water. Discovery presents new approach to medical imaging
This discovery is considered the first non-invasive technique for viewing living internal organs in animals.
Study co-author Mark Brongersma, a Stanford professor of material sciences and engineering and applied physics, emphasized the collaborative nature of the research, which brought together experts from various fields like materials science, neuroscience and physics.
While this research has so far only been tested on live mice, the possibilities for human medicine are exciting. If this technique could be adapted to humans, it could change the way doctors diagnose and treat various conditions.
For instance, instead of relying on invasive biopsies, doctors might be able to detect skin cancers, like melanoma, by simply looking through the skin. This technique could also make blood draws less painful by making it easier and quicker to locate veins – even fragile or thin veins, such as those in newborns, infants, the aged or patients who are scared of needles – and might even reduce the need for some CT scans or X-rays.
In addition to medical uses, this technology could have cosmetic applications as well. For instance, it could improve laser tattoo removal by helping to target tattoo pigments beneath the skin more precisely.
As scientists continue to explore the potential of tartrazine and similar dyes, this study represents a significant step toward new, less invasive ways to observe the living body – from patients needing medical imaging to those looking for easier, more precise cosmetic procedures.
Watch this video showing how applying a tartrazine solution to the skin of mice temporarily made it transparent .
This video is from the Daily Videos channel on Brighteon.com . More related stories:
Nearly half of FDA-approved AI-powered medical devices lack clinical validation data .
New study suggests going vegan for 8 weeks can help turn back your biological clock .
South Korean scientists discover how to use nanoparticles to control emotions, appetite via external magnetic field .
Scientists discovery that cancer drugs might help restore insulin production in patients with diabetes .
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Study suggests antidepressants might give memory a boost
Antidepressants have the potential to improve memory and thinking skills, a new study suggests. Photo by Adobe Stock/HealthDay News Antidepressants have the potential to improve memory and thinking skills, a new study suggests.
Some patients experienced a boost on brain tests after taking the SSRI antidepressant escitalopram (Lexapro), researchers report.
The drug appeared to affect a serotonin receptor in the brain called the 5HT4 receptor, according to results published recently in the journal Biological Psychiatry .
Serotonin is described as a “feel good” hormone, researchers said in background notes. Higher levels of serotonin in the brain contribute to a sense of well-being and have been shown to ease clinical depression. Related
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“It seems that the SSRI medication contributes to an improvement on cognitive function, at the same time as helping improve mood,” said lead investigator Vibeke Dam , a senior researcher in neurology and neurobiology with Copenhagen University Hospital in Denmark.
“Our work ties the improvement in cognitive function to the specific 5HT4 receptor and suggest that direct serotonin 4 receptor stimulation may be an important pro-cognitive target to consider in optimizing outcomes of antidepressant treatment,” Dam added in a journal news release. “It also reinforces the idea that serotonin is crucial to mood improvement.”
For the study, researchers scanned the brains of 90 depressed patients to measure 5HT4 receptor function in their brains. The patients also were tested for mood problems and cognitive abilities.
Then the patients were given daily escitalopram (Lexapro) for eight weeks. At the end of the study, 40 patients were rescanned and retested.
What did they find? The patients’ performance on cognitive tests had improved — particularly their ability to recall words — and this performance appeared to be linked to higher activity with the 5HT4 receptor.
“This work points to the possibility of stimulating this specific receptor so that we can treat cognitive problems, even aside from whether or not the patient has overcome the core symptoms of depression,” said lead researcher Dr. Vibe Froekjaer , a clinical professor of neuropsychiatry with Copenhagen University Hospital in Denmark.
The team’s next step will be to treat patients with drugs that specifically target the 5HT4 receptor, and then assess the effect on their brain function. Serotonin is found in the gut, and there are irritable bowel syndrome drugs that specifically bind to and stimulate 5HT4 receptors, researchers said.
Researchers also presented these findings Monday at the European College of Neuropsychopharmacology’s annual meeting in Milan.
The study “demonstrates the intimate role of brain 5HT4 receptors in cognitive function,” said Philip Cowen , a professor of psychopharmacology with the University of Oxford.
“This confirms recent work from Oxford showing that the 5HT4 receptor stimulant, prucalopride — a drug licensed for the treatment of constipation — improves memory in both healthy participants and people at risk of depression,” said Cowen, who was not involved in the study.
More information
The National Institutes of Health has more on antidepressants .
Copyright © 2024 HealthDay. All rights reserved.
Unexpected Brain Booster: Antidepressants Linked to Enhanced Cognitive Abilities
SSRIs may enhance verbal memory and cognitive performance by modifying serotonin receptor levels in the brain, offering dual benefits for treating depression. Credit: SciTechDaily.com Researchers have uncovered that SSRIs, specifically escitalopram, not only improve mood in depressed patients but also enhance cognitive functions such as verbal memory.
This improvement is linked to a reduction in the brain’s 5HT 4 serotonin receptors. Further studies aim to investigate drugs targeting these receptors to potentially treat cognitive deficits in depression, affirming the critical role of serotonin in both mood and cognitive functions. SSRI Antidepressants and Cognitive Enhancement
Antidepressants have the potential to improve certain cognitive functions, such as verbal memory, according to new research on SSRI (Selective Serotonin Reuptake Inhibitors). The scientists measured brain function in patients before and after taking the SSRI escitalopram and correlated this to a drop in the level of one of the serotonin receptors in the brain and to cognitive improvements during treatment. This work is presented for the first time at the ECNP Conference in Milan, after recent publication in the journal Biological Psychiatry. Serotonin’s Role in Well-being and Depression
Serotonin is often described as a ‘feel good’ chemical, and higher levels of serotonin circulating in the brain contribute to a sense of well-being, and can ease clinical depression in most sufferers. There are several serotonin receptors in the brain, and all will serve to regulate well-being by regulating circulating serotonin’s interaction with the brain. However, this work concentrated on only one serotonin receptor, the 5HT 4 receptor.
The researchers began by scanning the brains of 90 depressed patients, to measure the quantity of 5HT 4 receptor to which serotonin binds. At the same time, patients were given a series of tests to measure mood and cognitive abilities. Linking Cognitive Gains to SSRI Treatment
Patients were given daily doses of escitalopram, and at the end of an 8-week period, 40 patients were rescanned to measure the quantity of 5HT 4 receptors in the brain. The mood of the patients had improved, but the team also found that the levels of 5HT 4 receptor had dropped by around 9% possibly due to adaptations to increased levels of serotonin. When they asked these patients to undertake more cognitive tests, they found that their performance had improved, so that the less the 5HT 4 receptor had changed the better the cognitive outcome. This phenomenon was particularly prominent for the ability to recall words. Potential Implications and Future Research
“This is potentially significant” said researcher Vibeke Dam (Copenhagen University Hospital, Rigshospitalet, Denmark), “It seems that the SSRI medication contributes to an improvement on cognitive function, at the same time as helping improve mood. Our work ties the improvement in cognitive function to the specific 5HT 4 receptor and suggest that direct serotonin 4 receptor stimulation may be in important pro-cognitive target to consider in optimizing outcomes of antidepressant treatment. It also reinforces the idea that serotonin is crucial to mood improvement.
Co-researcher Vibe Froekjaer (Copenhagen University Hospital, Rigshospitalet, Denmark), added, “This is a first result, so we need to do a lot more work to look at the implications. Poor cognitive function is very hard to treat efficiently and may require extra treatment. This work points to the possibility of stimulating this specific receptor so that we can treat cognitive problems, even aside from whether or not the patient is has overcome the core symptoms of depression.”
The researchers note that this was a real-world study, so there is no placebo control.
The team’s next step is to treat patients with drugs that specifically stimulate the 5HT 4 receptor to see the effect on cognitive function; interestingly, serotonin is also found in the gut, and there are drugs available to treat irritable bowel syndrome that specifically bind to and stimulate 5HT 4 , which the team may repurpose in these trials. Expert Perspectives on Serotonin and Cognitive Functions
Commenting, Professor Philip Cowen, Professor of Psychopharmacology at the University of Oxford said:
“In the context of recent controversies about the role of brain serotonin in clinical depression, it is noteworthy that the PET studies of the Copenhagen Group provide unequivocal evidence that brain 5-HT4 receptors are decreased in unmedicated depressed patients. Their work also demonstrates the intimate role of brain 5-HT4 receptors in cognitive function. This confirms recent work from Oxford showing that the 5-HT4 receptor stimulant, prucalopride – a drug licensed for the treatment of constipation- improves memory in both healthy participants and people at risk of depression.”
This is an independent comment, Professor Cowen was not involved in this work.
Reference: “Effect of antidepressant treatment on 5-HT 4 receptor binding and associations with clinical outcomes and verbal memory in major depressive disorder” by Vibeke H. Dam, Kristin Köhler-Forsberg, Brice Ozenne, Søren V. Larsen, Cheng Teng Ip, Anders Jorgensen, Dea S. Stenbæk, Jacob Madsen, Claus Svarer, Martin B. Jørgensen, Gitte M. Knudsen and Vibe G. Frokjaer, 22 August 2024, Biological Psychiatry.
DOI: 10.1016/j.biopsych.2024.08.009
A cell biologist is investigating the balance of brain flexibility, stability
Andrea Gomez is fascinated by the brain’s ability to find the balance between stability and flexibility. One of the most remarkable things about the human brain is that it changes. A lot. This ability to reinvent itself, to morph, to strengthen some connections and let others fall away, captivates Andrea Gomez.
A molecular and cell biologist at the University of California, Berkeley, Gomez spends her time trying to figure out how the brain stays flexible, but not too flexible ( SN: 7/27/12).
The human brain operates on a knife’s edge, a slim, just-right compromise between flexibility and rigid structure, Gomez says. Too much plasticity would devolve into chaos. “We would never have a memory form. We would never learn anything,” she says. But too much rigidity would be equally calamitous. “Some of the most interesting questions, I find, is what mechanisms, what biological features, allow us to live at that edge.” Extreme Climate Survey
Science News is collecting reader questions about how to navigate our planet’s changing climate. What do you want to know about extreme heat and how it can lead to extreme weather events? Fill out our survey Gomez’s inquiries span from the tiny — for instance, minuscule conduits called synapses that sprout between nerve cells — to big shifts in behavior. This wide-ranging curiosity is one of her hallmarks as a scientist, says Peter Scheiffele, a neurobiologist at the University of Basel in Switzerland and her former postdoc adviser.
He remembers when Gomez, who had been studying the brain, became fascinated by the gut. She began experimenting with the idea that molecular instructions could help pattern the gut the same way they pattern the brain, but the work was stopped by COVID-19.
“I don’t see this as a story of a lack of success,” Scheiffele says. “I see it as the opposite — a story of genuine enthusiasm, motivation and, at some points, a certain randomness, but a creative randomness.” It’s a story of saying, “Hey, this is cool. I really want to poke at this and see if there is something exciting going on,’” Scheiffele says. “That to me is symbolic of how she often goes about science.”
Scheiffele says some scientists are linear thinkers who stick to a rigid plan. Gomez is more “blue sky, go out there and challenge yourself, challenge a problem,” he adds. She goes with optimism and says, “Let’s see.” In her lab, Andrea Gomez searches for signals that sculpt brain behavior. That “let’s see” energy has taken Gomez through plenty of big changes in her research directions. As an undergraduate at Colorado State University in Fort Collins, she studied crustacean molting, among other things. Then, as a graduate student at New York University, she ultimately shifted to brains, studying the plasticity of nerve cell connections.
While working in Scheiffele’s group as a postdoc, she and her colleagues made a surprising discovery about how certain synapses are built.
The discovery hinged on a process known as “splicing.” Cellular machinery doesn’t just copy information continuously and faithfully from DNA. These messages can get cut and recombined, or spliced, to form new versions of proteins. These spliced messages are “opportunities for something to be different,” Gomez says.
It turns out that, in the brains of mice at least, a version of a protein that results from a splicing event dramatically affects synapses of certain nerve cells. When that version of the protein was missing, these synapses weren’t as responsive as they should be, and mice flipped from being curious about new objects to avoiding them , the researchers reported in 2016 in Science .
The results “made us and many people in the field begin to think very differently about what splicing in the nervous system does,” says Scheiffele, a coauthor of the work. “It’s not some kind of fine-tuning tweaking. It can be a fundamental switch.”
These days, Gomez has a new focus. Instead of looking at how internal proteins enable change, she’s begun a project on an intriguing external way to shift the brain — psychedelic drugs.
Psychedelics are thought to open windows of plasticity in the brain in ways that scientists don’t fully understand. One way this flexibility may emerge is through splicing, Gomez suspects. A single dose of psilocybin led to thousands of splicing events in mice’s brains that didn’t happen without the drug, Gomez and her colleagues have found in preliminary research. “This, to me, is such a rich repertoire to discover new mechanisms of plasticity,” she says, “and that’s really my goal.”
Psychedelic drugs’ effects on the brain are still, by and large, a mystery, says Gordon Fishell, a developmental neurobiologist at Harvard Medical School and the Broad Institute. “Anything that so profoundly affects your sense of self, being, identity, consciousness is fundamental to how we think of how the brain functions,” he says.
Other post-psychedelic changes abound: There are changes in gene activity and reduction of rigid structures around nerve cells that have been implicated in memory storage, called perineuronal nets ( SN: 10/20/15 ). Some of the biggest changes happen in nerve cell activity in a part of the brain that handles perception.
Gomez is from Las Cruces, N.M., and is a member of the Laguna Pueblo tribe. “I heard about psychedelics before I started working on it, from Indigenous perspectives, all the way back to high school.” Soon after she arrived at Berkeley and began setting up her new lab, a new colleague floated the idea of teaming up to study how psychedelics make the brain more flexible — another instance of Gomez being open to change, and saying, “Let’s see.”
Questions or comments on this article? E-mail us at feedback@sciencenews.org | Reprints FAQ Citations
L. Traunmüller. A.M. Gomez, et al . Control of neuronal synapse specification by a highly dedicated alternative splicing program . Science . Vol. 352, May 20, 2016, p. 982. doi: 10.1126/science.aaf2397.
Laura Sanders is the neuroscience writer. She holds a Ph.D. in molecular biology from the University of Southern California. We are at a critical time and supporting climate journalism is more important […]
Scientists discover microplastics in the olfactory bulbs of the human brain
Scientists have found microplastics in many parts of the human body, including the brain. MEM Studio/Stocksy Microplastics are common in people’s everyday environments, and research is ongoing on microplastics in the human body.
Recent study findings revealed that microplastics can be present in the brain’s olfactory bulbs.
While there is limited research, there could be certain health implications, such as an increased risk for neurodegenerative diseases because of exposure to microplastics.
Microplastics permeate the environment, and human beings are frequently exposed to them. Research is ongoing about how microplastics accumulate in people and the related health risks.
A study published in JAMA Network Open confirmed that microplastics can be present in the olfactory bulbs of the brain in people, based on their analysis of 15 deceased people.
While more research can help confirm these findings, the results support that the olfactory pathway, which has to do with smell, could be a way for microplastics to enter the brain. Microplastics traveling to the human brain
The National Oceanic and Atmospheric Administration notes that “microplastics are small plastic pieces less than five millimeters long.”
Evidence suggests that microplastics may travel to several areas of the human body, such as the bloodstream and the colon . However, as researchers of this study note, “While MPs [microplastics] have been detected in various human tissues, their presence in the human brain has not been documented.”
This study was an opportunity to look for the presence of microplastics in the olfactory bulbs of the human brain. The olfactory bulbs are a critical component of people’s ability to smell. Researchers of this study note that the olfactory pathway from the neurons in the nose to the brain could allow certain substances into the brain.
For this study, researchers examined the olfactory bulbs of fifteen deceased individuals between the ages of thirty-three and one hundred. Before death, all individuals were residents of São Paulo for over five years, and all had undergone coroner autopsy.
The researchers gathered data on underlying diseases and what the participants did for a living from the next of kin. Researchers excluded individuals who had had neurosurgery. They used two stillborns as negative controls but could only analyze one sample from this group. Among participants, two showed evidence of previous ischemic stroke, and one had a subarachnoid hematoma because of a ruptured aneurysm.
The researchers used several methods to avoid outside contamination of samples with microplastics. Overall, researchers identified microplastics in eight of the fifteen individuals. The most common type of polymer they identified was polypropylene, and particles were the most common shape identified. Microplastics entering the body through the nose?
The results highlight microplastics’ presence in another body organ and suggest that the olfactory pathway may be a way for microplastics to reach the brain.
Tracey Woodruff, PhD , professor and director of Environmental Research and Translation for Health (EaRTH) Center at the University of California, San Francisco, who was not involved in the study, commented with her thoughts on the study to Medical News Today:
“It was very thorough. It wasn’t very big…so it’s not as large as some of the other studies. It’s really concerning that we’re seeing microplastics measured in brain tissue, note not all of the brain tissue, but we shouldn’t be surprised given that microplastics have been measured in all the other human tissues that have been examined to date. [M]icroplastics are everywhere and they’re also in us.”
Heather A. Leslie, PhD , an independent scientist specializing in nanoplastic and microplastic analysis and problem-solving based in Amsterdam, who was also not involved in the study, also commented with her thoughts on the study to Medical News Today:
“This study is an important first step in understanding what kind of real-world microplastic accumulation we can expect in human olfactory tissue. The study identified a very low number of plastic particles (between 1 and 4) in half of the cadavers tested, though it is difficult to compare these data to other studies because no microplastics concentrations are reported per gram tissue.”
“More sensitive detection techniques and more rigorous quality control should be applied in the future to see if the results can be replicated,” she added. Can microplastics affect brain health?
More research is required to understand the full health implications of microplastic exposure and its influence on the brain.
“Finding one or two microplastics in parts of the brain does not directly prove there are health implications in a given population, but these data do compel us to find out. Measuring health effects requires additional work to collect the toxicological effect data that tell us which doses are dangerous and which are not,” Leslie noted.
However, microplastic exposure could contribute to certain brain-related issues.
The study authors note that some microplastics are associated with particulate matter, and exposure to particulate matter could contribute to problems like dementia. In addition, exposure to particulate matter and microplastics could lead to problems in brain development.
“A component of particulate matter air pollution is definitely made up of microplastics. We know that exposure to particulate matter air pollution is associated with neurodegenerative effects. [T]here’s different studies showing that it can increase the risk of neurodegenerative diseases like Alzheimer’s. [T]he fact that we’re finding microplastics in the brain means that that can disturb brain function which could increase the risk of neurodegenerative disorders,” Woodruff said. How to limit exposure to microplastics
This research does have some limitations that warrant caution and continued research.
All of the deceased individuals had lived in the same area for over five years, meaning that future studies could include data from people in other regions. It also only included a small number of participants, and a great majority of the participants were male, which does limit the findings. It’s possible that the unique health and life circumstances of these people could have impacted the results. Reports from next kin could be inaccurate as well.
The study also only included adults in a specific age range, so additional research with other age demographics could be useful. […]
The Power Within by Corey Daniels book available for only $2.99
Mind has both conscious and subconscious halves. These are likened to a driver and the truck he drives. The driver plans the destination and observes road conditions, while the truck provides motive power. Your subconscious mind is like the truck and it only goes in the direction in which is a steered. This can be the road or off a cliff. Likewise, the consciousness paints a picture of what the world is and what your goals are and the subconscious acts on them through emotion, physical response and energy, whether these are correct, rational images or false negative ones. The subconscious is also like an emotional reservoir which your body and mind draw responses from to external stimuli.
The Power Within lays out a method of programming your subconscious and tapping into the Holy Spirit, God voice or what the Greeks called the daimon (godman).