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Study outlines cases of people successfully treating cancer with fenbendazole protocol
At a time when turbo cancers are alarming doctors and patients around the world thanks to the widespread use of risky COVID-19 vaccines, the need for effective cancer treatments has never been more pressing. Although this disease is notoriously difficult to treat, some people are finding success with a treatment known as fenbendazole.
This anti-parasitic drug has been getting some attention for its potential in treating various types of cancer, particularly pancreatic cancer, which is known for being highly aggressive and having a low survival rate. There have been a number of early studies showing that it can be helpful , although further research is needed to reach a more definitive conclusion.
The medication is currently used primarily by vets to treat gastrointestinal parasites in animals, such as hookworms, roundworms and whip worms, but research suggesting that it has the power to inhibit the growth of cancer cells and spur the death of cancer cells by inhibiting glucose uptake and disrupting the formation of microtubules could change the way cancer is treated in the future.
Some people are already trying it out with varying degrees of success. One popular protocol is the Stanford Fenbendazole Protocol. On X, Dr. William Makis shared several examples of the protocol in action taken from a Case Series published by the Department of Medicine at Stanford University Medical Center.
One of the cases involves a 72-year-old man who was suffering from stage 4 cancer of the urethra who developed metastases in the lymph node, brain and lung. After failing a number of treatments, including radiotherapy, pembrolizumab, paclitaxel and carboplatin, not to mention six cycles of cisplatin and gemcitabine, he switched to a regimen of 1000 milligrams of fenbendazole orally three times per week, along with vitamin E, curcumin and CBD oil. A CT scan later showed his tumor shrinking by 2 cm before eventually disappearing entirely.
Another case involved a 63-year-old man who was suffering from stage 4 renal cell carcinoma with metastases to the pancreas and bone and a 5.3 cm mass. Three lines of chemotherapy were unsuccessful, but he was able to reach remission after taking 1000 milligrams of fenbendazole three times a week; his tumors also shrink considerably.
The third case involved a 63-year-old woman who was suffering from stage 4 bladder cancer and had a 7.5 cm tumor. She used chemotherapy and fenbendazole in conjunction with one another, and a follow-up CT found no sign of the disease after treatment.
Makis noted the importance of new treatments as we deal with a “tsunami of cancer,” particularly turbo cancers caused by mRNA vaccines, pointing out that the protocol is largely suppressed by search engines.
“Every cancer patient MUST have an Alternative Treatment approach, which can be taken concurrently with conventional chemotherapy, radiation therapy or immunotherapy, as the Stanford Group showed,” he wrote. Global cancer deaths to rise by 93% by 2050 among men
A new study that was published in the journal Cancer shows that cancer cases and deaths are expected to surge by the year 2050 among men, especially those aged 65 and older. The study, which was carried out by Australian researchers, projected that the overall cancer cases in men will rise from 10.3 million in 2022 to 19 million in 2054 in a jump of 84%, while deaths from cancer are projected to climb from 5.4 million in 2022 two 10.5 million by 2050 for a rise of 93%. When looking at those older than 65, cancer deaths were projected to rise by 117%.
Sources for this article include:
X.com
Healthline.com
Nature.com
CNN.com
Synaptic Quality Key to Age Related Memory Preservation
Summary: A recent study reveals that the quality, not the quantity, of synapses in the brain is crucial for preserving memory in older adults. Researchers found that larger dendritic spine head diameters in the temporal cortex correlate with better episodic memory performance, challenging the long-held belief that memory decline is primarily due to synapse loss.
This discovery suggests that therapies targeting synaptic strength may improve memory in aging and Alzheimer’s patients. The findings emphasize the potential for cognitive preservation through enhancing existing synaptic connections.
Key Facts:
> Synapse Quality: Larger dendritic spine head diameters in the temporal cortex are linked to better memory performance.
Memory Preservation: Synaptic strength is more crucial than the number of synapses for memory retention in old age.
Therapeutic Potential: Targeting pathways that enhance synaptic strength could improve memory in older adults and Alzheimer’s patients.
Source: University of Alabama
Over the course of life, memory fades with varying degrees, robbing older people of the ability to recollect personal experiences. This progressive, nearly inevitable process has long been hypothesized as a consequence of nature’s removal of dendritic spines, a key component of synapses, from brain neurons as they age.
A study published in Science Advances led by researchers at the University of Alabama at Birmingham and Rush University Medical Center, Chicago, Illinois, now provides evidence that the preservation of past life experiences is maintained by the quality — not the quantity — of synapses in old age. Even in older individuals, people age 80, 90 or 95, there is still enough plasticity in synapse formation to retain memory. Credit: Neuroscience News “This is a paradigm breaker,” said Jeremy Herskowitz, Ph.D., associate professor in the UAB Department of Neurology and corresponding author of the study.
“For 35 years, the predominant dogma was that memory decline is mediated predominantly by loss of dendritic spine, which are a surrogate for synapses. As we age from 40 through 85, there is natural loss of dendritic spines and synapses, which is completely normal.
“This natural loss can contribute to the lack of cognitive sharpness that we all feel as we age. However, we demonstrate that, even though there is synapse loss, the ones that are left can compensate for that loss.”
Herskowitz says this has an enormous implication. “Even in older individuals, people age 80, 90 or 95, there is still enough plasticity in synapse formation to retain memory. This means a therapy to remodel dendritic spines and synapses could dramatically facilitate memory as you age or if you are experiencing memory impairment due to Alzheimer’s disease dementia.”
The study was made possible by the Religious Orders Study and Rush Memory and Aging Project, or ROSMAP, at Rush University. ROSMAP enrolls Catholic nuns, priests and brothers age 65 or older, who are without known dementia at time of enrollment. Participants receive medical and psychological evaluations each year and agree to donate their brains after death.
Herskowitz and colleagues studied postmortem brain samples from 128 ROSMAP participants. The participants had an average age of 90.5 years at the time of death, with variable cognitive performance scores and Alzheimer’s disease-related neuropathology.
They all had undergone yearly cognitive testing for episodic memory, visuospatial ability/perceptual orientation, perceptual speed, semantic memory, and working memory. The study included two samples from each brain, one from the temporal cortex, which has structures vital for long-term memory, and one from the frontal premotor cortex.
After staining the brain samples, photographing thin slices and building three-dimensional digital reconstructions of 55,521 individual dendritic spines on 2,157 neurons, researchers used two statistical methods, one employing innovative machine learning, to see if any of 16 different spine morphology measurements correlated with any of 17 different measures of brain function, age and Alzheimer’s disease neuropathology. One of the brain function measures was episodic memory — the ability to remember everyday events and past personal experiences.
For neurons from the temporal cortex, researchers found that dendritic spine head diameter, but not the quantity of spines, improved prediction of episodic memory in models containing β-amyloid plaque scores, neurofibrillary tangle pathology and sex.
Larger head diameters were associated with better episodic memory performance, supporting the emerging hypothesis that, in the temporal cortex, synaptic strength is more critical than quantity for memory in old age.
“Targeting pathways that maintain spine head diameter or synaptic strength, rather than pathways that maintain or generate new spines or synapses, could potentially yield greater therapeutic benefits for older adults in preclinical phases of Alzheimer’s disease,” Herskowitz said.
A dendrite is a branched extension from a neuron body that receives impulses from other neurons. Each dendrite can have thousands of small protrusions called spines. The head of each spine can form a contact point called a synapse to receive an impulse sent from the axon of another neuron. Dendritic spines can rapidly change shape or volume while forming new synapses, part of the process called brain plasticity. Creating or eliminating synapses is a fundamental mechanism of brain function.
Collecting the tens of thousands of spine measurements took two and a half years. This painstaking work started in 2019 and continued through the COVID-19 pandemic, as UAB researchers worked under COVID restrictions, Herskowitz says.
Co-first authors of the study, “Dendritic spine head diameter predicts episodic memory performance in older adults,” are Courtney K. Walker and Evan Liu, UAB Department of Neurology.
Other authors are Kelsey M. Greathouse, Ashley B. Adamson, Julia P. Wilson, Emily H. Poovey, Kendall A. Curtis, Hamad M. Muhammad and Audrey J. Weber, UAB Department of Neurology; David A. Bennett, Rush University Medical Center; Nicholas T. Seyfried, Emory University School of Medicine; and Christopher Gaiteri, SUNY Upstate Medical University, Syracuse, New York.
Funding: Support came from National Institutes of Health grants NS061788, AG067635, AG061800, AG054719, AG063755, AG068024, AG10161, AG72975, AG15819, AG17917, AG46152 and AG61356. About this synaptic plasticity research news
Author: Jeffrey Hansen
Source: University of Alabama
Contact: Jeffrey Hansen – University of Alabama Image: The image is credited to Neuroscience News Original Research : Closed access. “ Dendritic spine head diameter predicts episodic memory performance in older adults ” by Jeremy Herskowitz et […]
Light and Sound Therapy Maintains Myelin in Alzheimer’s
Summary: A new study finds that 40Hz light and sound therapy helps maintain myelin, a crucial brain structure, in Alzheimer’s patients. This therapy, which protects neurons and supports brain function, could offer new treatment avenues for neurodegenerative diseases.
Researchers discovered that this stimulation enhances neural connections and reduces harmful inflammation. The therapy also shows potential for treating other conditions involving myelin loss, such as multiple sclerosis.
Key Facts:
> 40Hz sensory stimulation preserves myelin in Alzheimer’s patients.
The therapy enhances neural connections and reduces inflammation.
Potential applications include treatment for multiple sclerosis.
Source: Picower Institute at MIT
Early-stage trials in Alzheimer’s disease patients and studies in mouse models of the disease have suggested positive impacts on pathology and symptoms from exposure to light and sound presented at the “gamma” band frequency of 40 Hz.
A new study zeroes in on how 40Hz sensory stimulation helps to sustain an essential process in which the signal-sending branches of neurons, called axons, are wrapped in a fatty insulation called myelin. Often called the brain’s “white matter,” myelin protects axons and insures better electrical signal transmission in brain circuits. Amorim and Tsai’s team found that 40Hz light and sound not only preserved myelination in the brains of cuprizone-exposed mice, it also appeared to protect oligodendrocytes (the cells that myelinate neural axons), sustain the electrical performance of neurons, and preserve a key marker of axon structural integrity. Credit: Neuroscience News “Previous publications from our lab have mainly focused on neuronal protection,” said Li-Huei Tsai, Picower Professor in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences at MIT and senior author of the new study in Nature Communications . Tsai also lead’s MIT’s Aging Brain Initiative. “But this study shows that it’s not just the gray matter, but also the white matter that’s protected by this method.”
This year Cognito Therapeutics, the spin-off company that licensed MIT’s sensory stimulation technology, published phase II human trial results in the Journal of Alzheimer’s Disease indicating that 40Hz light and sound stimulation significantly slowed the loss of myelin in volunteers with Alzheimer’s.
Also this year Tsai’s lab published a study showing that gamma sensory stimulation helped mice withstand neurological effects of chemotherapy medicines, including by preserving myelin. In the new study, members of Tsai’s lab led by former postdoc Daniela Rodrigues Amorim used a common mouse model of myelin loss—a diet with the chemical cuprizone— to explore how sensory stimulation preserves myelination.
Amorim and Tsai’s team found that 40Hz light and sound not only preserved myelination in the brains of cuprizone-exposed mice, it also appeared to protect oligodendrocytes (the cells that myelinate neural axons), sustain the electrical performance of neurons, and preserve a key marker of axon structural integrity.
When the team looked into the molecular underpinnings of these benefits, they found clear signs of specific mechanisms including preservation of neural circuit connections called synapses; a reduction in a cause of oligodendrocyte death called “ferroptosis;” reduced inflammation; and an increase in the ability of microglia brain cells to clean up myelin damage so that new myelin could be restored.
“Gamma stimulation promotes a healthy environment,” said Amorim who is now a Marie Curie Fellow at the University of Galway in Ireland. “There are several ways we are seeing different effects.”
The findings suggest that gamma sensory stimulation may help not only Alzheimer’s disease patients but also people battling other diseases involving myelin loss, such as multiple sclerosis, the authors wrote in the study.
Maintaining myelin
To conduct the study, Tsai and Amorim’s team fed some male mice a diet with cuprizone and gave other male mice a normal diet for six weeks. Halfway into that period, when cuprizone is known to begin causing its most acute effects on myelination, they exposed some mice from each group to gamma sensory stimulation for the remaining three weeks.
In this way they had four groups: completely unaffected mice, mice that received no cuprizone but did get gamma stimulation, mice that received cuprizone and constant (but not 40Hz) light and sound as a control, and mice that received cuprizone and also gamma stimulation.
After the six weeks elapsed, the scientists measured signs of myelination throughout the brains of the mice in each group. Mice that weren’t fed cuprizone maintained healthy levels, as expected. Mice that were fed cuprizone and didn’t receive 40Hz gamma sensory stimulation showed drastic levels of myelin loss.
Cuprizone-fed mice that received 40Hz stimulation retained significantly more myelin, rivaling the health of mice never fed cuprizone by some, but not all, measures.
The researchers also looked at numbers of oligodendrocytes to see if they survived better with sensory stimulation. Several measures revealed that in mice fed cuprizone, oligodendrocytes in the corpus callosum region of the brain (a key point for the transit of neural signals because it connects the brain’s hemispheres) were markedly reduced. But in mice fed cuprizone and also treated with gamma stimulation, the number of cells were much closer to healthy levels.
Electrophysiological tests among neural axons in the corpus callosum showed that gamma sensory stimulation was associated with improved electrical performance in cuprizone-fed mice who received gamma stimulation compared to cuprizone-fed mice left untreated by 40Hz stimulation.
And when researchers looked in the anterior cingulate cortex region of the brain, they saw that MAP2, a protein that signals the structural integrity of axons, was much better preserved in mice that received cuprizone and gamma stimulation compared to cuprizone-fed mice who did not.
Molecular mechanisms
A key goal of the study was to identify possible ways in which 40Hz sensory stimulation may protect myelin.
To find out, the researchers conducted a sweeping assessment of protein expression in each mouse group and identified which proteins were differentially expressed based on cuprizone diet and exposure to gamma frequency stimulation. The analysis revealed distinct sets of effects between the cuprizone mice exposed to control stimulation and cuprizone-plus-gamma mice.A highlight of one set of effects was the increase in MAP2 in gamma-treated cuprizone-fed mice. A highlight of another set was that cuprizone mice who received control stimulation […]
Study reveals ways in which 40Hz sensory stimulation may preserve brain’s ‘white matter’
Early-stage trials in Alzheimer’s disease patients and studies in mouse models of the disease have suggested positive impacts on pathology and symptoms from exposure to light and sound presented at the “gamma” band frequency of 40 Hz. A new study zeroes in on how 40Hz sensory stimulation helps to sustain an essential process in which the signal-sending branches of neurons, called axons, are wrapped in a fatty insulation called myelin. Often called the brain’s “white matter,” myelin protects axons and insures better electrical signal transmission in brain circuits.
“Previous publications from our lab have mainly focused on neuronal protection,” said Li-Huei Tsai, Picower Professor in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences at MIT and senior author of the new study in Nature Communications . Tsai also lead’s MIT’s Aging Brain Initiative. “But this study shows that it’s not just the gray matter, but also the white matter that’s protected by this method.”
This year Cognito Therapeutics, the spin-off company that licensed MIT’s sensory stimulation technology, published phase II human trial results in the Journal of Alzheimer’s Disease indicating that 40Hz light and sound stimulation significantly slowed the loss of myelin in volunteers with Alzheimer’s. Also this year Tsai’s lab published a study showing that gamma sensory stimulation helped mice withstand neurological effects of chemotherapy medicines, including by preserving myelin. In the new study, members of Tsai’s lab led by former postdoc Daniela Rodrigues Amorim used a common mouse model of myelin loss — a diet with the chemical cuprizone — to explore how sensory stimulation preserves myelination.
Amorim and Tsai’s team found that 40Hz light and sound not only preserved myelination in the brains of cuprizone-exposed mice, it also appeared to protect oligodendrocytes (the cells that myelinate neural axons), sustain the electrical performance of neurons, and preserve a key marker of axon structural integrity. When the team looked into the molecular underpinnings of these benefits, they found clear signs of specific mechanisms including preservation of neural circuit connections called synapses; a reduction in a cause of oligodendrocyte death called “ferroptosis;” reduced inflammation; and an increase in the ability of microglia brain cells to clean up myelin damage so that new myelin could be restored.
“Gamma stimulation promotes a healthy environment,” said Amorim who is now a Marie Curie Fellow at the University of Galway in Ireland. “There are several ways we are seeing different effects.”
The findings suggest that gamma sensory stimulation may help not only Alzheimer’s disease patients but also people battling other diseases involving myelin loss, such as multiple sclerosis, the authors wrote in the study.
Maintaining myelin
To conduct the study, Tsai and Amorim’s team fed some male mice a diet with cuprizone and gave other male mice a normal diet for six weeks. Halfway into that period, when cuprizone is known to begin causing its most acute effects on myelination, they exposed some mice from each group to gamma sensory stimulation for the remaining three weeks. In this way they had four groups: completely unaffected mice, mice that received no cuprizone but did get gamma stimulation, mice that received cuprizone and constant (but not 40Hz) light and sound as a control, and mice that received cuprizone and also gamma stimulation.
After the six weeks elapsed, the scientists measured signs of myelination throughout the brains of the mice in each group. Mice that weren’t fed cuprizone maintained healthy levels, as expected. Mice that were fed cuprizone and didn’t receive 40Hz gamma sensory stimulation showed drastic levels of myelin loss. Cuprizone-fed mice that received 40Hz stimulation retained significantly more myelin, rivaling the health of mice never fed cuprizone by some, but not all, measures.
The researchers also looked at numbers of oligodendrocytes to see if they survived better with sensory stimulation. Several measures revealed that in mice fed cuprizone, oligodendrocytes in the corpus callosum region of the brain (a key point for the transit of neural signals because it connects the brain’s hemispheres) were markedly reduced. But in mice fed cuprizone and also treated with gamma stimulation, the number of cells were much closer to healthy levels.
Electrophysiological tests among neural axons in the corpus callosum showed that gamma sensory stimulation was associated with improved electrical performance in cuprizone-fed mice who received gamma stimulation compared to cuprizone-fed mice left untreated by 40Hz stimulation. And when researchers looked in the anterior cingulate cortex region of the brain, they saw that MAP2, a protein that signals the structural integrity of axons, was much better preserved in mice that received cuprizone and gamma stimulation compared to cuprizone-fed mice who did not.
Molecular mechanisms
A key goal of the study was to identify possible ways in which 40Hz sensory stimulation may protect myelin.
To find out, the researchers conducted a sweeping assessment of protein expression in each mouse group and identified which proteins were differentially expressed based on cuprizone diet and exposure to gamma frequency stimulation. The analysis revealed distinct sets of effects between the cuprizone mice exposed to control stimulation and cuprizone-plus-gamma mice.
A highlight of one set of effects was the increase in MAP2 in gamma-treated cuprizone-fed mice. A highlight of another set was that cuprizone mice who received control stimulation showed a substantial deficit in expression of proteins associated with synapses. The gamma-treated cuprizone-fed mice did not show any significant loss, mirroring results in a 2019 Alzheimer’s 40Hz study that showed synaptic preservation. This result is important, the researchers wrote, because neural circuit activity, which depends on maintaining synapses, is associated with preserving myelin. They confirmed the protein expression results by looking directly at brain tissues.
Another set of protein expression results hinted at another important mechanism: ferroptosis. This phenomenon, in which errant metabolism of iron leads to a lethal buildup of reactive oxygen species in cells, is a known problem for oligodendrocytes in the cuprizone mouse model. Among the signs was an increase in cuprizone-fed, control stimulation mice in expression of the protein HMGB1, which is a marker of ferroptosis-associated damage that triggers an inflammatory response. Gamma stimulation, however, […]
Study links 6 contaminant metals in urine to increased heart disease and mortality risk
Tags: badhealth , badpollution , badscience , cadmium , cobalt , copper , discoveries , Ecology , environment , health science , heart disease , heart health , Heavy metals , longevity , men’s health , metals , poison , real investigations , research , toxins , tungsten , uranium , women’s health , zinc Researchers from Columbia University have found that individuals with high levels of six metals in their urine – cadmium, cobalt, copper, tungsten, uranium and zinc – face a 66 percent higher risk of mortality. In addition, these individuals posted a 29 percent increase of developing cardiovascular disease (CVD) .
In their study published in the journal Circulation on August 1, the researchers stated that evidence is increasingly showing that involuntary environmental exposures, including contaminant metals, are significant modifiable risk factors for both clinical and subclinical CVD and all-cause mortality. These findings and insights can guide and help develop the creation of innovative preventive strategies to enhance and improve cardiovascular health.
Heavy metals are elements and compounds that can negatively impact health. While small amounts of many metals are necessary for life, excessive levels can be toxic. Common heavy metals that people are exposed to include aluminum, antimony, arsenic, barium, beryllium, cadmium, cesium, copper, lead, mercury, nickel, thallium, tungsten and uranium. (Related: Heavy metal toxicity symptoms explained: Are you poisoned? )
Increasing levels of pollution and the use of industrial chemicals have led to increased exposure and raised the dangers and threat of heavy metal toxicity – greatly endangering child development and overall health and well-being. High levels of these toxic metals in body tissues and the brain can lead to significant development and neurological issues.
Research has shown that exposure to certain metals can be linked to CVD and increased risk of death. However, previous studies focused mainly on arsenic, cadmium and lead. (Related: Heavy metal toxicity is a hidden epidemic .) Cadmium, cobalt, copper, tungsten, uranium and zinc linked to coronary artery calcification
This study aimed to explore how urinary levels of various metals relate to CVD and overall mortality among a diverse group of U.S. adults as part of the government-sponsored Multi-Ethnic Study of Atherosclerosis.
The researchers expanded their focus beyond arsenic, cadmium and lead to include metals like tungsten and uranium, which aren’t essential for the body but may be harmful. They also looked at cobalt, copper and zinc, which are essential in small amounts but can be toxic in excess.
Cadmium, cobalt, copper, tungsten, uranium and zinc were chosen because they are linked to coronary artery calcification, a sign of artery damage from fatty deposits.
The study involved nearly 6,600 participants from cities such as Baltimore, Chicago, Los Angeles, New York, St. Paul and the Winston-Salem area of North Carolina, with an average age of 62 years. About 53 percent of the participants were female. Their urine metal levels were measured between 2000 and 2001 and tracked until December 2019.
Researchers used statistical models to analyze the relationship between urinary levels of cadmium, tungsten, uranium (non-essential metals) and cobalt, copper and zinc (essential metals) with CVD and mortality rates. They also examined how combinations of these metals affected survival over 10 years.
Over the study period, 1,162 participants developed CVD and 1,844 died. When comparing the highest to the lowest levels of these metals, the risk ratios for developing cardiovascular disease and dying from any case were as follows: Cadmium: 1.25 for CVD, 1.68 for mortality
Cobalt: 1.24 for CVD, 1.37 for mortality
Copper: 1.42 for CVD, 1.50 for mortality
Tungsten: 1.20 for CVD, 1.16 for mortality
Uranium: 1.32 for CVD, 1.32 for mortality
Zinc: 1.21 for CVD, 1.38 for mortality
The study found a clear link between higher levels of cadmium and copper and increased risks for both endpoints. The overall survival probability decreased with higher baseline urinary levels of cadmium, cobalt, copper and zinc.
The research suggests that higher levels of these metals in urine are associated with an increased risk of CVD and higher mortality rates. These insights could help in developing new strategies to improve heart health and prevent cardiovascular issues.
Watch this video discussing heavy metal toxicity .
This video is from the Daily Videos channel on Brighteon.com . More related stories:
Cadmium poisoning signs and symptoms: Are you being poisoned by this heavy metal?
Detox heavy metals from your body with these 10 foods .
Stolen cobalt-60 proves how easily dirty bomb materials can be acquired and deployed .
Copper toxicity associated with depression, schizophrenia and other disorders .
Heavy metal tungsten linked to leukemia clusters in children .
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Researchers discover dual benefits of naturally occurring supplement on sleep and gut health
Credit: Miriam Alonso from Pexels National University of Singapore (NUS) nutritionists have found that 5-Hydroxytryptophan (5-HTP) supplementation can improve sleep quality in Singaporean older adults, particularly in individuals with poor sleep patterns, and manage their gut microbiome composition.
Ensuring good sleep quality is an integral part of achieving good health. However, a mental health study published in 2022 reported that close to 17% of older adults aged 65 and above in Singapore are suffering from poor sleep quality, which has been linked to worse health outcomes, such as a greater risk of chronic diseases and cognitive impairment.
There is growing evidence of the association between gut microbiota composition and sleep quality. Additionally, there are pharmaceutical sleep aids available to help poor sleepers achieve a good night’s sleep.
However, such aids may induce adverse side effects , including digestive problems and headaches. Dietary supplements, such as a naturally occurring amino acid, 5-HTP, are available, but its efficacy on sleep quality in older adults is unclear.
Through a 12-week clinical trial on 30 older adults, aged 65 and over, NUS researchers set out to evaluate the impact of 5-HTP supplementation on sleep quality and gut microbiota composition on older adults.
The research team was led by Assistant Professor Kim Jung Eun from the Department of Food Science and Technology (NUS FST) under the NUS Faculty of Science, and the study was conducted in collaboration with Adjunct Associate Professor Johnson Fam from the Department of Psychological Medicine at the NUS Yong Loo Lin School of Medicine.
Based on the results of the clinical trial, the NUS team discovered that supplementation of 5-HTP can improve sleep quality in Singaporean older adults and this improvement was predominantly observed in poor sleepers, which could be linked to the modulation of their gut microbiome composition. The team’s findings were published in the journal Clinical Nutrition . Exploring the link between sleep and gut health
Dr. Clarinda Nataria Sutanto, an Instructor at NUS FST who is the first author of the paper, said, “5-HTP is a naturally occurring amino acid that the body converts into serotonin, a chemical that acts as a neurotransmitter in the brain. Supplementation with 5-HTP can enhance sleep quality and promote a state of sleepiness by modulating the levels of these neurotransmitters involved in regulating the sleep-wake cycle.”
Asst Prof Kim added, “It is also worth noting that this sleep-promoting effect was mostly observed in individuals with poor sleep quality and this finding supports the use of alternative, safer dietary strategies over medication for improving sleep.”
The researchers also analyzed the biological samples collected from the participants to understand the effect of 5-HTP supplementation on gut health. The results of their analysis revealed that among poor sleepers, there was a significant increase in gut microbiota diversity and abundance of gut bacteria, which is linked to improved gut health. From these results, the researchers postulate that the improvement in sleep quality could be attributed to the boost in gut health among poor sleepers after supplementation with 5-HTP.
“Results from this study provide scientific evidence supporting the beneficial effects of 5-HTP supplementation on sleep quality via modulation of the gut-brain axis, highlighting the bidirectional interaction between the gastrointestinal tract and the nervous system ,” said Asst Prof Kim.
Following the promising results of this clinical trial, the researchers aim to explore other dietary strategies, such as comparing the effect of protein intake from different sources and the impact of other food items which may affect gut health on enhancing sleep quality. The NUS team also hopes to expand their scope of study to include younger individuals who experience poor sleep quality due to stress, anxiety, and excessive use of electronic devices in their daily lives.
More information: Clarinda Nataria Sutanto et al, The impact of 5-hydroxytryptophan supplementation on sleep quality and gut microbiota composition in older adults: A randomized controlled trial, Clinical Nutrition (2024). DOI: 10.1016/j.clnu.2024.01.010
Provided by National University of Singapore
Eating for necessity or pleasure? There is a brain circuit for that
People eat either because they are hungry or for pleasure, even in the absence of hunger. While hunger-driven eating is fundamental for survival, pleasure-driven feeding may accelerate the onset of obesity and associated metabolic disorders. A study published in Nature Metabolism reveals neural circuits in the mouse brain that promote hunger-driven feeding and suppress pleasure-driven eating. The findings open new possibilities for developing strategies to combat obesity.
“Ideal feeding habits would balance eating for necessity and for pleasure, minimizing the latter,” said co-corresponding author Dr. Yong Xu , professor of pediatrics – nutrition and associate director for basic sciences at the USDA/ARS Children’s Nutrition Research Center at Baylor College of Medicine. “In this study we identified a group of neurons that regulates balanced feeding in the brain.”
Previous studies have highlighted the role of neurons identified by the GABAergic proenkephalin (Penk) marker, an endogenous opioid hormone, on feeding and body weight balance. However, their contribution to regulating hunger- and pleasure-driven feeding had not been elucidated.
In this study, Xu and his colleagues showed that activation of Penk neurons in the brain region called diagonal band of Broca (DBB) of male mice supports an ideal feeding pattern, increasing hunger-driven feeding while reducing pleasure-driven eating.
“I was surprised by this finding,” Xu said. “We and other groups had previously shown that certain groups of neurons affect both feeding types in the same way – they either increase or decrease both types. Here we found that activating DBB-Penk neurons has opposite effects in the two types of feeding, they increase hunger-driven feeding while decreasing eating for pleasure.”
The researchers investigated the mechanism mediating these opposite effects. They discovered that DBB-Penk neurons project into two different brain areas, one regulates hunger-driven feeding and the other controls pleasure-driven eating.
“A subset of DBB-Penk neurons that projects to the paraventricular nucleus of the hypothalamus is preferentially activated upon food presentation during fasting periods, facilitating hunger-driven feeding,” Xu said. “On the other hand, a separate subset of DBB-Penk neurons that projects to a different brain region, the lateral hypothalamus, is preferentially activated when detecting high-fat, high-sugar (HFHS) foods and inhibits their consumption. This is the first study to show a neural circuit that is activated by a reward, HFHS, but leads to terminating instead of continuing the pleasurable activity.”
Strikingly, mice in which the entire DBB-Penk population had been eliminated, when given free choice of chow and HFHS diets, reduced consumption of chow but increased intake of the HFHS diet, resulting in accelerated development of obesity and metabolic disturbances.
“Our findings indicate that the development of obesity is associated with impaired function of some of these brain circuits in mice,” Xu said. “We are interested in further investigating molecular markers within the circuits that could be suitable targets for treatment of human diseases such as obesity.”
Other contributors to this work include Hailan Liu, Yongxiang Li, Meng Yu, Olivia Z. Ginnard, Kristine M. Conde, Mengjie Wang, Xing Fang, Hesong Liu, Longlong Tu, Na Yin, Jonathan C. Bean, Junying Han, Yongjie Yang, Qingchun Tong, Benjamin R. Arenkiel, Chunmei Wang and co-corresponding author Yang He, at Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. The authors are affiliated with one of the following institutions: Baylor College of Medicine, Baylor’s USDA/ARS Children’s Nutrition Research Center, Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital and University of Texas Health Science Center at Houston.
This study was supported by grants from the USDA/CRIS (51000-064-01S, 3092-51000-062-04(B)S), Texas Children’s Research Scholar funds, American Heart Association (23POST1030352) and NIH NIDDK (1F32DK134121-01A1). Brain Neurons A photo of cows being herded by a man on a horse
Study reveals ways in which 40Hz sensory stimulation may preserve brain’s ‘white matter’
by Massachusetts Institute of Technology Green staining indicates myelination in these mouse brain cross sections. The brain that received 40Hz light and sound stimulation (right) shows significantly more myelin in four brain regions (insets): the cortex (CTX), the anterior commissure (AC), the corpus callosum (CC), and the striatum (STR) than in mice who did not receive 40Hz stimulation. Credit: Tsai Laboratory/MIT Picower Institute Early-stage trials in Alzheimer’s disease patients and studies in mouse models of the disease have suggested positive impacts on pathology and symptoms from exposure to light and sound presented at the gamma band frequency of 40 Hz.
A new study zeroes in on how 40Hz sensory stimulation helps to sustain an essential process in which the signal-sending branches of neurons, called axons, are wrapped in a fatty insulation called myelin. Often called the brain’s “white matter,” myelin protects axons and insures better electrical signal transmission in brain circuits.
“Previous publications from our lab have mainly focused on neuronal protection,” said Li-Huei Tsai, Picower Professor in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences at MIT and senior author of the new study in Nature Communications . Tsai also leads MIT’s Aging Brain Initiative. “But this study shows that it’s not just the gray matter, but also the white matter that’s protected by this method.”
This year Cognito Therapeutics, the spin-off company that licensed MIT’s sensory stimulation technology, published phase II human trial results in the Journal of Alzheimer’s Disease indicating that 40Hz light and sound stimulation significantly slowed the loss of myelin in volunteers with Alzheimer’s.
This year, Tsai’s lab also published a study showing that gamma sensory stimulation helped mice withstand neurological effects of chemotherapy medicines, including by preserving myelin.
In the new study, members of Tsai’s lab led by former postdoc Daniela Rodrigues Amorim used a common mouse model of myelin loss—a diet with the chemical cuprizone—to explore how sensory stimulation preserves myelination.
Amorim and Tsai’s team found that 40Hz light and sound not only preserved myelination in the brains of cuprizone-exposed mice, it also appeared to protect oligodendrocytes (the cells that myelinate neural axons), sustain the electrical performance of neurons, and preserve a key marker of axon structural integrity. When the team looked into the molecular underpinnings of these benefits, they found clear signs of specific mechanisms including preservation of neural circuit connections called synapses; a reduction in a cause of oligodendrocyte death called “ferroptosis;” reduced inflammation; and an increase in the ability of microglia brain cells to clean up myelin damage so that new myelin could be restored.
“Gamma stimulation promotes a healthy environment,” said Amorim, who is now a Marie Curie Fellow at the University of Galway in Ireland. “There are several ways we are seeing different effects.”
The findings suggest that gamma sensory stimulation may help not only Alzheimer’s disease patients, but also people battling other diseases involving myelin loss, such as multiple sclerosis, the authors wrote in the study. Maintaining myelin
To conduct the study, Tsai and Amorim’s team fed a group of male mice a diet with cuprizone and gave another group of male mice a normal diet for six weeks. Halfway into that period, when cuprizone is known to begin causing its most acute effects on myelination, they exposed some mice from each group to gamma sensory stimulation for the remaining three weeks. In this way, they had four groups: completely unaffected mice, mice that received no cuprizone but did get gamma stimulation, mice that received cuprizone and constant (but not 40Hz) light and sound as a control, and mice that received cuprizone and also gamma stimulation. To assess the number of immature and mature oligodendrocytes in the corpus callosum in mice fed cuprizone and given 40 Hz stimulation (right), compared to mice fed cuprizone and given constant stimulation as a control, researchers measured the marker PDGFRa (green) and APCCC1 (red). The 40Hz group exhibited a signficantly higher number of each type of oligodendrocytes. Credit: Tsai Laboratory/MIT Picower Institute After the six weeks elapsed, the scientists measured signs of myelination throughout the brains of the mice in each group. Mice that weren’t fed cuprizone maintained healthy levels, as expected. Mice that were fed cuprizone and didn’t receive 40Hz gamma sensory stimulation showed drastic levels of myelin loss. Cuprizone-fed mice that received 40Hz stimulation retained significantly more myelin, rivaling the health of mice never fed cuprizone by some, but not all, measures.
The researchers also looked at numbers of oligodendrocytes to see if they survived better with sensory stimulation. Several measures revealed that in mice fed cuprizone, oligodendrocytes in the corpus callosum region of the brain (a key point for the transit of neural signals because it connects the brain’s hemispheres) were markedly reduced. But in mice fed cuprizone and also treated with gamma stimulation, the number of cells were much closer to healthy levels.
Electrophysiological tests among neural axons in the corpus callosum showed that gamma sensory stimulation was associated with improved electrical performance in cuprizone-fed mice who received gamma stimulation compared to cuprizone-fed mice left untreated by 40Hz stimulation. And when researchers looked in the anterior cingulate cortex region of the brain, they saw that MAP2, a protein that signals the structural integrity of axons, was much better preserved in mice that received cuprizone and gamma stimulation compared to cuprizone-fed mice who did not. Molecular mechanisms
A key goal of the study was to identify possible ways in which 40Hz sensory stimulation may protect myelin.
To investigate, the researchers conducted a sweeping assessment of protein expression in each mouse group and identified which proteins were differentially expressed based on cuprizone diet and exposure to gamma frequency stimulation. The analysis revealed distinct sets of effects between the cuprizone mice exposed to control stimulation and cuprizone-plus-gamma mice.
A highlight of one set of effects was the increase in MAP2 in gamma-treated cuprizone-fed mice. A highlight of another set was that cuprizone mice who received control stimulation showed a substantial deficit in expression of proteins associated with synapses. The gamma-treated cuprizone-fed mice did not […]
South Korean scientists discover how to use nanoparticles to control emotions, appetite via external magnetic field
08/07/2024 // Belle Carter // 590 Views
Tags: badhealth , badmedicine , badscience , big government , biotechnology , brain function , brain health , breakthrough , computing , Dangerous , discoveries , future science , future tech , Glitch , health science , information technology , inventions , manipulation , medical experiments , mind body science , mind control , Nano-MIND , nanoparticles , nanotechnology , neuroscience Globalist-“sponsored” scientists are so obsessed with controlling the mind that they conducted a study where a remote magnet would be able to manipulate the brain – even one’s appetite – without any invasive procedure performed.
Researchers at South Korea’s Institute for Basic Science (IBS) are in the very early stages of development of hardware that utilizes nanoparticles to control the minds of mice. It is a brain remote control that they claimed is “long-range” and “large-volume” and switches using magnetic fields.
According to the “science experts,” the technology dubbed Nano-MIND (Magnetogenetic Interface for NeuroDynamics), allowed researchers to control the emotions and appetites of mice from afar and could be used to treat neurological disorders like depression. They tested the “innovation” by inducing “maternal” instincts in their female test subjects. In another test, the researchers exposed a test group of lab mice to magnetic fields designed to reduce appetite, leading to a 10-percent loss in body weight, or about 4.3 grams.
The scientists manipulated a complex network of over 100 billion neurons by magnetically twisting a tiny actuator to pull or push nanoparticles implanted in the mice’s brains. According to studies, this network is crucial for understanding cognition, emotion and social behavior.
“This is the world’s first technology to freely control specific brain regions using magnetic fields,” said Dr. Cheon Jinwoo, director of South Korea’s IBS Center, who helped spearhead the new effort. “We expect it to be widely used in research to understand brain functions, sophisticated artificial neural networks, two-way brain-computer interface technologies, and new treatments for neurological disorders.”
There have been numerous “mind control” experiments on animals over the years, the Sun reported, “But this is the first that hasn’t involved invasive surgery and bulky external systems, which has instead allowed mice the freedom of movement.”
In an op-ed that came with the said study published in Nature Nanotechnology , senior scientist at Spain’s Instituto de Neurociencias Dr. Felix Leroy said that the concept of using magnetic fields to manipulate biological systems has been well established. “It has been applied in various fields,” he noted, “like in magnetic resonance imaging [MRI], transcranial magnetic stimulation and magnetic hyperthermia for cancer treatment.”
However, he cautioned against rushing too soon to human testing . “Further studies are needed to assess potential cumulative effects, including neuroadaptation or neurotoxicity,” Leroy advised.
A nanoparticle is a small particle that ranges between one to 100 nanometres in size, which is undetectable by the human eye and even smaller than the wavelengths of visible light which are between 400 and 700 nanometres. A special electron microscope or microscope with lasers is needed to observe them. Studies involving nanoparticles are branches of nanotechnology that is famously relied upon by the fictional Marvel character Tony Stark, aka Iron Man. Korean, U.S. scientists create a brain implant that could be controlled using a smartphone
In a separate effort by South Korea and the United States, supported by grants from the National Research Foundation of Korea, the National Institutes of Health, the National Institute on Drug Abuse, and Mallinckrodt Professorship, another innovation was tested to control the brain. A soft neural implant, capable of delivering multiple drugs and color lights, was discovered to manipulate neural circuits using a smartphone.
In the study that was published in Nature Biomedical Engineering , the researchers said the tiny implant is the first wireless neural device capable of speeding up efforts to uncover brain diseases, such as Parkinson’s, Alzheimer’s, addiction, depression and pain.
“The wireless neural device enables chronic chemical and optical neuromodulation that has never been achieved before,” said lead author Raza Qazi, a researcher with the Korea Advanced Institute of Science and Technology (KAIST) and the University of Colorado Boulder .
Co-author Michael Bruchas, a professor of anesthesiology and pain medicine and pharmacology at the University of Washington School of Medicine , said this technology allowed them to better dissect the neural circuit basis of behavior “and how specific neuromodulators in the brain tune behavior in various ways,” he said. “We are also eager to use the device for complex pharmacological studies, which could help us develop new therapeutics for pain, addiction, and emotional disorders.”
The device uses Lego-like replaceable drug cartridges and powerful Bluetooth low-energy to deliver drugs and light to specific neurons of interest.
According to the scientists, this technology significantly overshadows conventional neuroscience methods, which usually involve rigid metal tubes and optical fibers. Though some efforts have addressed adverse tissue response by incorporating soft probes and wireless platforms, the previous solutions were limited by their inability to deliver drugs for long periods as well as their bulky and complex control setups.
Controlled with a simple user interface on a smartphone, the device can create a specific combination or precise sequencing of light and drug deliveries in any implanted target animal without the need to be inside the laboratory. With this device, researchers could easily set up fully automated animal studies where the behavior of one animal could positively or negatively affect behavior in other animals by conditional triggering of light and/or drug delivery.
“This revolutionary device is the fruit of advanced electronics design and powerful micro and nanoscale engineering,” said Jae-Woong Jeong, a professor of electrical engineering at KAIST. “We are interested in further developing this technology to make a brain implant for clinical applications.” (Related: Neuralink receives FDA approval to implant brain chip in second patient .)
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Study reveals key brain cells help resist food temptations in favor of exercise
In a recent study published in the journal Nature Neuroscience , researchers investigate the role of hypocretin/orexin neurons (HONs) in temptation-resistant voluntary exercise (TRVE).
Study: Orexin neurons mediate temptation-resistant voluntary exercise. Image Credit: ViDI Studio / Shutterstock.com The neurology of obesity
Obesity is a major public health issue worldwide, with many individuals under-exercising and overconsuming highly palatable foods (HPF). The neurological mechanisms that may be involved in the exercise-HPF consumption association remain unclear despite chronic HPF overconsumption being shown to adversely influence cognitive and neural measures.
The lateral hypothalamic region is involved in motivation; however, its involvement in controlling food intake and calorie balance is unknown. Lateral hypothalamic HONs release neurotransmitters called orexins/hypocretins, which activate particular G-protein-based receptor molecules throughout the brain. About the study
In the current study, researchers use murine models to investigate the role of orexin and HONs on the decision to exercise or eat. The influence of pharmacological or optogenetic interruption of HON activity on exercise or HPF intake was also examined in multiple-choice settings.
Voluntary-type wheel running was used to model human health-promoting exercise. During ten-minute trials, mice were offered eight alternatives, including a wheel to run on and a “milkshake bar” with a strawberry-flavored milkshake. Several groups of mice were subjected to these tests, including control mice and those with suppressed orexin systems due to almorexant (ALMO) treatment or genetic alteration.
The appetitive and consummatory stages of food consumption and exercise were investigated by providing mechanistic and neuroeconomic explanations of exercise choice. To this end, mice were placed in eight-arm mazes with options such as moving wheels, novel objects, water, light and dark zones, and food. One arm was left vacant or held very appealing food. Ten-minute sessions were used to assess initial decision-making processes while minimizing fatigue and satisfaction effects.
The behavioral and microstructural processes of orexin-based TRVE were examined by assessing the frequency and length of running and eating.
Decision-making processes involved in TRVE, specifically murine engagement in wheel running or HPF consumption from a neutral zone, were also studied. To better understand the impact of HONs on HPF usage, mice were housed in a cage containing both alternatives to reduce appetitive place preferences.
Real-time fiber photometry recordings from the lateral hypothalamus allowed the researchers to investigate the fast dynamics of HONs during TRVE. Linear mixed-effects models (LMEM) were used with HON signaling as response variables and HPF licking, wheel run, and non-wheel locomotive activities as input variables. To investigate the significance of normal HON activity variations, persistent HON-selective optostimulation was used to create an artificially elevated state. Study findings
with a blocked orexin system were more likely to choose HPF over exercise, whereas mice with intact orexin systems spent twice as much time running on the wheel and half the time eating food.
These findings indicate that orexin does not control the time spent in physical activity or eating; however, it is crucial for selecting between activity and eating when both options are available. Without orexin, mice abandoned exercising in favor of the strawberry milkshake.
Limiting meal selections to regular chow meals showed that mice spent time between spinning the wheel and eating. After introducing HPF to the choices, mice spent significantly less time eating chow, whereas running wheel usage and occupation remained the same. Reduced running wheel use in mice treated with ALMO was associated with increased time spent in the highly palatable food area and HPF consumption. ALMO treatment significantly limited the occupancy and utilization of both running wheel areas when they were available. Thus, orexin likely mediates between eating and running without altering appetitive or consummatory urges towards either activity.
HON signals significantly changed in mice moving through a labyrinth, with HON activity negatively associated with licking and positively associated with wheel and non-wheel running speed. Optostimulation decreased measurements of activities typically associated with low HON activity, thus indicating that HON activity variations are critical for preferring exercise over eating. a, Mice (n = 71) explored an eight-arm maze containing distinct alternatives at the end of each arm. Mouse location was video-tracked over a 10-min period. b, Heatmaps of an example mouse displaying a shift in time spent in the chow arm (left) toward the HPF, when available (right). c, In the maze version lacking the HPF option (black), mice spent the most time in the wheel and chow arms. In the maze version with the HPF option available (teal), mice spent the most time in the wheel and HPF arms. The lines represent the means; the shaded regions represent the s.e.m. of n = 71 mice. d, Total time spent in the wheel arm in the absence and presence of the HPF option (paired t-test: t70 = −0.683, P = 0.497, n = 71 mice). e, Total distance traveled on the wheel in the absence and presence of the HPF option (paired t-test: t70 = 1.514, P = 0.134, n = 71 mice). f, Total distance run in the xy plane of the maze outside the wheel in the absence and presence of the HPF option (paired t-test: t70 = −1.147, P = 0.256, n = 71 mice). NS, not significant. Box plots: the center line is the median, the box edges are the top and bottom quartiles, the whiskers are minimum and maximum. a , Mice (n = 71) explored an eight-arm maze containing distinct alternatives at the end of each arm. Mouse location was video-tracked over a 10-min period. b , Heatmaps of an example mouse displaying a shift in time spent in the chow arm (left) toward the HPF, when available (right). c , In the maze version lacking the HPF option (black), mice spent the most time in the wheel and chow arms. In the maze version with the HPF option available (teal), mice spent the most time in the wheel and HPF arms. The lines represent the means; the shaded regions represent the s.e.m. of n = 71 mice. d , Total time spent in the wheel arm in the absence and presence of the HPF option (paired t-test: t […]
Researchers pioneer noninvasive measurement of gene expression at target locations in the brain
Striatum region (left) in rodent brain with opened blood-brain barrier. Green fluorescent protein expressed in striatum region in rodent brain (right) in response to induced neuronal activity. Credit: Laboratory for Noninvasive Imaging/Rice University The ability to alter or prevent the expression of faulty genes in the brain could be leveraged as a powerful therapeutic against neurodegenerative disease. However, the molecular underpinnings of the living brain are still largely inaccessible, hampering progress on such promising therapeutics.
Available options for probing the brain are not quite up to the task. The most effective way to record molecular information from multiple genes is biopsy ⎯ an invasive, high-risk procedure.
A study published today in Science Advances describes new technology developed by the Rice University lab of bioengineer Jerzy Szablowski that could be a game changer for brain-based gene therapy . Called “Recovery of Markers through InSonation,” or REMIS, the new noninvasive tool can measure expression of gene therapy or endogenous genes in specific brain regions.
“Our limited ability to measure gene expression has significant consequences for the future of gene therapy,” Szablowski said. “For example, in most cases it is not possible to noninvasively confirm whether gene therapy has successfully reached the brain, how long it stays there and which brain regions are being affected by it. Our study shows it is possible to measure gene expression and gene therapy delivery in specific brain regions with a relatively simple ultrasound procedure.”
REMIS builds on prior work by Szablowski and collaborators that focused on engineered molecules known as released markers of activity (RMAs). With the RMA platform, the researchers introduced a synthetic gene expression reporter to the brain, which in turn produced a protein that could cross from the brain into the bloodstream, where it could be easily retrieved and measured with a blood test with exquisite sensitivity: RMA expression in as few as 12 neurons could be reliably detected in blood.
The downside to this initial version of the technology was that the markers crossed the brain-blood barrier indiscriminately and thus could not be traced back to specific brain regions. REMIS fixed the issue by using ultrasound to ferry engineered protein markers into the bloodstream only from targeted locations in the brain.
“Here we made markers that cannot cross these blood vessels until they are stimulated with ultrasound,” Szablowski said.
Another advantage for REMIS is that it can also measure naturally occurring gene expression. One example is c-Fos, a gene that is used as a marker of neuronal activity. This highlights the potential of REMIS not only for gene therapy but also as a diagnostic and research tool.
“We are particularly excited about this technology, especially since our work has already led to a funded clinical trial with our colleagues at Baylor College of Medicine and MD Anderson Cancer Center,” Szablowski said.
The trial will involve using focused ultrasound to release proteins present in the brain of patients with Parkinson’s disease into the bloodstream, which could provide new insights into the molecular mechanisms involved in the disease. However, Szablowski said a more immediate application for REMIS is monitoring the success of gene delivery in the brain.
“Gene therapy is one of the most exciting frontiers in medicine, but we need to have tools to know whether the gene therapeutic reaches the part of the brain it’s supposed to and works in the ways intended,” Szablowski said. “REMIS provides a nonsurgical option to do so, potentially utilizing the gene therapeutic itself as a marker. This is a big advantage since methods such as PET scans entail the clinical development of new probes for every new therapeutic.”
More information: Joon Pyung Seo et al, Acoustically targeted measurement of transgene expression in the brain, Science Advances (2024). DOI: 10.1126/sciadv.adj7686 Citation : Researchers pioneer noninvasive measurement of gene expression at target locations in the brain (2024, August 7) retrieved 8 August 2024 from https://medicalxpress.com/news/2024-08-noninvasive-gene-brain.html
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Scientists Claim Brain Chemicals Are Linked to Blood Pressure Regulation
Your “love hormone” can impact your blood pressure at times when your oxygen level is low.
Recently, scientists have recently identified two brain-produced chemicals, including oxytocin, which is popularly known as the love hormone. The team concluded that they can affect our blood pressure during hypoxia.
According to them, this discovery could pave the way for new therapeutic approaches to managing heart-related diseases, often linked to sleep deprivation and low oxygen states. The Brainstem’s Influence on Blood Pressure
(Photo : Mockup Graphics from Unsplash) Your love hormone can not only affect your social bonding and attachment to someone but also your blood pressure, according to the latest study. Research indicates that oxytocin and another hormone, corticotropin-releasing hormone (CRH), significantly affect blood pressure. Oxytocin is well-known for its role in social bonding and attachment, while CRH is critical in stress responses, behavior, and inflammation.
A recent study aimed to investigate how these neurohormones influence the brainstem, the brain structure responsible for regulating vital functions such as blood pressure, according to Interesting Engineering.
Related Article: Breathing Traffic-Related Air Linked to Sudden Spike in Blood Pressure That Lasts 24 Hours Sleep Deprivation and Low Oxygen Levels
Dr. David Kline, a professor at the University of Missouri College of Veterinary Medicine, led the study exploring the relationship between brain chemicals and blood pressure. He noted that sleep deprivation, often resulting in periods of low oxygen levels (hypoxia), triggers the body to increase breathing to restore oxygen levels. This reflexive response is crucial in understanding how hypoxia affects blood pressure.
“It also causes a reflex for our blood pressure to go up to get that oxygenated blood to go where it needs to go,” Kline said in an interview with Live Science. Experimental Study on Lab Rats
To delve deeper into this phenomenon, researchers conducted experiments on lab rats, dividing them into two groups: one maintained under normal oxygen levels and the other subjected to low-oxygen conditions.
Over 10 days, scientists observed the effects of oxytocin and CRH on the rats’ brainstems, analyzing neuron activity and chemical releases. Findings and Implications
The study revealed that hypoxic rats exhibited increased brainstem activity and elevated blood pressure compared to those in normal oxygen conditions.
Notably, there was a significant rise in the release of chemicals from the paraventricular nucleus (PVN) and an increase in the number of receptors in the brainstem. These changes suggest that oxytocin and CRH play a pivotal role in regulating blood pressure under low-oxygen conditions. Future Therapeutic Avenues
Dr. Kline highlighted that these findings could lead to new therapeutic approaches. He thought that this study could open possibilities that clinicians and drug firms could pick up.
However, he also cautioned that it will take time to translate these discoveries into effective treatments for human patients.
The identification of oxytocin and CRH as key players in blood pressure regulation under hypoxic conditions opens exciting possibilities for developing new treatments for heart-related diseases. As research progresses, these findings may significantly impact how we approach blood pressure management and overall cardiovascular health.
The study can be found in the Journal of Physiology.
In other news, Tech Times reported that the loss of visual sensitivity can predict dementia 12 years before diagnosis.
Read Also: Neuralink Achieves Major Milestone: Second Brain Implant Successful, Elon Musk Says Joseph Henry
Exercise or snack? How our brain decides
by ETH Zurich Credit: CC0 Public Domain Should I go and exercise, or would I rather go to the café and enjoy a delectable strawberry milkshake? Until now, what exactly happens in our brain when we make this decision has been a mystery to science, but researchers at ETH Zurich have found the solution. They have deciphered which brain chemical and which nerve cells mediate this decision: the messenger substance orexin and the neurons that produce it.
These neuroscientific fundamentals are relevant because many people don’t get enough exercise. Most of us have probably already decided once or even several times to skip exercising in favor of one of the numerous alternative temptations of daily life. According to the World Health Organization, 80% of adolescents and 27% of adults don’t get enough exercise. And obesity is increasing at an alarming rate not only among adults but also among children and adolescents. Focus on orexin
“Despite these statistics, many people manage to resist the constantly present temptations and get enough exercise,” says Denis Burdakov, Professor of Neuroscience at ETH Zurich. “We wanted to know what it is in our brain that helps us make these decisions.”
In their experiments with mice , the researchers were able to show that orexin plays a key role in this process. It’s one of over a hundred messenger substances that are active in the brain. Other chemical messengers , such as serotonin and dopamine, were discovered a long time ago and their role has largely been decoded. The situation for orexin is different: Researchers discovered it relatively late, around 25 years ago, and they are now clarifying its functions step by step. Burdakov is one of the scientists who have devoted their efforts to studying orexin. Existing knowledge can’t explain the choice
“In neuroscience, dopamine is a popular explanation for why we choose to do some things but avoid others,” says Burdakov. This brain messenger is critical for our general motivation. “However, our current knowledge about dopamine does not easily explain why we decide to exercise instead of eating,” the scientist continues. “Our brain releases dopamine both when we eat and when we exercise, which does not explain why we choose one over the other.”
To find out what does explain this, the researchers devised a sophisticated behavioral experiment for mice, which were able to choose freely from among eight different options in ten-minute trials. These included a wheel they could run on and a “milkshake bar” where they could enjoy a standard strawberry-flavored milkshake.
“Mice like a milkshake for the same reason people do: It contains lots of sugar and fat and tastes good,” says Burdakov. Less time at the milkshake bar
In their experiment, the scientists compared different groups of mice: one made up of normal mice and one in which the mice’s orexin systems were blocked, either with a drug or through genetic modification of their cells.
The mice with an intact orexin system spent twice as much time on the running wheel and half as much time at the milkshake bar as the mice whose orexin system had been blocked. Interestingly, however, the behavior of the two groups didn’t differ in experiments in which the scientists only offered the mice either the running wheel or the milkshake.
“This means that the primary role of the orexin system is not to control how much the mice move or how much they eat,” Burdakov says. “Rather, it seems central to making the decision between one and the other, when both options are available.” Without orexin, the decision was strongly in favor of the milkshake, and the mice gave up exercising in favor of eating. Helping people who do little exercise
The ETH Zurich researchers expect that orexin may also be responsible for this decision in humans; the brain functions involved here are known to be practically the same in both species.
“It will now be a matter of verifying our results in humans,” says Daria Peleg-Raibstein, group leader at ETH Zurich. She led the study together with Denis Burdakov. This could involve examining patients who have a restricted orexin system for genetic reasons—this is the case in around one in two thousand people. These people suffer from narcolepsy (a sleeping disorder). Another possibility would be to observe people who receive a drug that blocks orexin. Such drugs are authorized for patients with insomnia.
“If we understand how the brain arbitrates between food consumption and physical activity , we can develop more effective strategies for addressing the global obesity epidemic and related metabolic disorders,” says Peleg-Raibstein.
In particular, interventions could be developed to help overcome exercise barriers in healthy individuals and those whose physical activity is limited. However, Burdakov points out that these would be important questions for scientists involved in clinical research in humans. He and his group have dedicated themselves to basic neuroscientific research. Next he wants to find out how the orexin neurons interact with the rest of the brain when making decisions like the one between exercise and snacking.
More information: Orexin neurons mediate temptation-resistant voluntary exercise, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01696-2
Provided by ETH Zurich
‘Feel-Good Neurotransmitter’ Dopamine May Improve Memory Of Alzheimer’s Patients, Study Suggests
Topline
Researchers have found that increasing dopamine production in mice with Alzheimer’s disease improves their memory, a process they’re hopeful can be replicated in humans, though more testing for a better human alternative must be done. Woman hugging her older mother.getty Key Facts
A research team from Japan’s RIKEN Center for Brain Science tested the new treatment method, boosting the production of dopamine in the brains of mice with Alzheimer’s in the hopes of increasing levels of an enzyme called neprilysin.
Prior research has shown neprilysin can reduce the production of protein pieces called beta-amyloid, which causes the formation of plaque around brain neurons—one of the earliest indicators of Alzheimer’s disease—and the research team had previously found the neurotransmitter dopamine increases levels of neprilysin.
The scientists were able to continuously activate the neurons in the mice’s brains that produce dopamine, and after eight weeks the mice had significantly fewer plaques in their brains, according to a new study published Tuesday in Science Signaling.
Next, levodopa —a Parkinson’s drug used as a dopamine replacement—was given to some of the mice because, although the drug has severe side effects, boosting dopamine production in humans with a medication is a more feasible treatment method than genetically manipulating growth like the researchers did with the mice.
The medication was given for three months and led to an increase in neprilysin and a subsequent decrease in beta-amyloid, and the mice that were given this treatment performed better on memory tests than the placebo group that wasn’t treated with the drug. What Side Effects Does Levodopa Have?
The researchers believe levodopa—also known as L-DOPA—is a good starting point to begin research on human treatment of boosting dopamine production in Alzheimer’s patients, but it may not be the best option in the long run because it has “serious side effects” in some Parkinson’s patients. Some of the most common side effects include dizziness, nausea, confusion, hallucination, psychosis, low blood pressure, agitation and delusion, according to StatPearls research . Long-term use can lead to complications like irreversible motor function changes, which affects roughly 50% of patients who take the drug for five to 10 years. Because of these side effects, “our next step is to investigate how dopamine regulates neprilysin in the brain, which should yield a new preventive approach that can be initiated at the preclinical stage of Alzheimer’s disease,” Dr. Watamura Naoto, first author of the study and researcher with the RIKEN Center for Brain Science, said in a statement. What Is Dopamine?
Dopamine—also known as the “feel-good neurotransmitter”—is a hormone and a type of neurotransmitter in the brain that’s used by the nervous system to send messages to the nerves, according to the Cleveland Clinic. It plays an important role in the brain’s reward system because it’s released by the brain when a person does something that’s pleasurable. This rush of dopamine causes a person to seek more of that feeling, which can lead to behaviors like drug and alcohol addiction and overeating, according to the Cleveland Clinic. Research has shown the hormone may play a big part in dementia because low dopamine levels may indicate early signs of Alzheimer’s disease and other forms of dementia. Big Number
6.7 million. That’s how many Americans aged 65 years or older had Alzheimer’s in 2023, according to the Alzheimer’s Association. Around one in nine people aged 65 or older have Alzheimer’s. Tangent
Erectile dysfunction drugs like Viagra may also be key Alzheimer’s treatments, according to a Neurology study published in February. The researchers found participants who were prescribed erectile dysfunction drugs were 18% less likely to develop Alzheimer’s than their counterparts who weren’t. The types of drugs used in the study are called phosphodiesterase type-5 inhibitors, and the researchers believe PDE5Is may reduce Alzheimer’s risk because some forms of the drugs can improve brain health by increasing blood flow to the brain, and reducing the amount of energy neurons consumed in the brain. Further Reading
Erectile Dysfunction Drugs Like Viagra May Reduce Alzheimer’s Risk, Study Finds (Forbes) Forbes Daily: Join over 1 million Forbes Daily subscribers and get our best stories, exclusive reporting and essential analysis of the day’s news in your inbox every weekday.
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Boost your brain: The power of a healthy diet
Credit: Pixabay/CC0 Public Domain Recent research has shown that our diet plays a crucial role in maintaining not just our physical well-being, but also our brain health. A diet high in sugars and processed foods can weaken brain function and negatively impact mental health. Your brain requires healthy foods like fruits, vegetables, whole grains, fish and lean meat to keep it running smoothly.
The brain and gut share significant connections through a pathway called the gut-brain axis. The vagus nerve links your brain and stomach, allowing them to communicate directly. Your gastrointestinal tract is sometimes nicknamed the “second brain” due to this connection. This link can be seen in our daily lives; whenever you experience “butterflies in your stomach,” you are feeling that connection firsthand.
Additionally, the microbiome full of microscopic organisms living in our gut can significantly impact our mood and mental health . These organisms thrive when you consume a diet rich in fiber from whole foods.
Take advantage of the relationship between your diet and brain function and eat these “brain foods” to increase your mental alertness and mood. Berries: Berries, blueberries in particular, are rich in flavanols which are linked to improved cognitive function. Flavanols help improve blood flow to the brain. Additionally, the antioxidants in blueberries help protect brain cells from oxidative stress and inflammation. Research has shown a link between regular consumption of berries and decreased risk of certain cognitive disorders such as Alzheimer’s and dementia.
Fish: Omega-3 fatty acids play an important role in promoting a healthy brain. They reduce inflammation and improve communication between brain cells. Omega-3 also helps promote the growth and repair of brain tissue which enhances cognitive function. These healthy fats can be found in seafood like salmon, sardines, mackerel, tuna, cod and oysters.
Leafy greens: Leafy greens are a staple of any healthy diet due to their high nutritional content. Spinach, arugula, kale and collards are rich in vitamins A and C and are high in fiber and folate. Research has shown that regular consumption of leafy greens may lead to a slower rate of cognitive decline and improved memory as you age. Try adding these nutritional powerhouses to whole grain pasta, soups and smoothies to sneak in those extra nutritional benefits.
Nuts: Nuts like walnuts, pistachios and almonds are beneficial to your overall brain health . Almonds are known to help improve memory. Pistachios can help with inflammation and may help with cognition. Walnuts are rich in antioxidants and DHA, a fatty acid that may improve learning ability.
Taking care of your brain health also means taking care of your gut. A healthy and balanced microbiome is connected to reduced risk of various mental health disorders and improved memory and cognition. Care for your gut health by enjoying these foods.
Probiotic foods: Probiotic foods help produce a healthy microbiome, which is responsible for producing chemicals like serotonin and dopamine. These compounds help regulate mood and support brain health. Probiotic foods include yogurt, kimchi, buttermilk, fermented vegetables like sauerkraut, and some cheeses. Studies have shown that regular consumption of probiotic foods is linked to reduced risk of anxiety and depression and enhances memory and learning abilities.
Prebiotic foods: Prebiotic foods such as garlic, onions, and bananas help to nourish beneficial gut bacteria, and in turn, support brain health. These foods help with the production of compounds like short chain fatty acids that play an important role in reducing inflammation to support brain function . To maintain a healthy gut and protect your brain, fuel your microbiome by eating plenty of fiber from fruits and vegetables, whole grains, and legumes like beans or chickpeas. Adults should aim for 25–30 grams per day.
Provided by University of Kentucky
Boost your brain: The power of a healthy diet
Published 3:30 pm Friday, August 2, 2024
By Special to The Advocate-Messenger
UK Healthcare
Recent research has shown that our diet plays a crucial role in maintaining not just our physical wellbeing, but also our brain health. A diet high in sugars and processed foods can weaken brain function and negatively impact mental health. Your brain requires healthy foods like fruits, vegetables, whole grains, fish and lean meat to keep it running smoothly.
The brain and gut share significant connections through a pathway called the gut-brain axis. The vagus nerve links your brain and stomach, allowing them to communicate directly. Your gastrointestinal tract is sometimes nicknamed the “second brain” due to this connection. This link can be seen in our daily lives; whenever you experience “butterflies in your stomach,” you are feeling that connection firsthand.
Additionally, the microbiome full of microscopic organisms living in our gut can significantly impact our mood and mental health. These organisms thrive when you consume a diet rich in fiber from whole foods.
Take advantage of the relationship between your diet and brain function and eat these “brain-foods” to increase your mental alertness and mood.
Berries : Berries, blueberries in particular, are rich in flavanols which are linked to improved cognitive function. Flavanols help improve blood flow to the brain. Additionally, the antioxidants in blueberries help protect brain cells from oxidative stress and inflammation. Research has shown a link between regular consumption of berries and decreased risk of certain cognitive disorders such as Alzheimer’s and dementia.
Fish : Omega-3 fatty acids play an important role in promoting a healthy brain. They reduce inflammation and improve communication between brain cells. Omega-3 also helps promote the growth and repair of brain tissue which enhances cognitive function. These healthy fats can be found in seafood like salmon, sardines, mackerel, tuna, cod and oysters.
Leafy greens : Leafy greens are a staple of any healthy diet due to their high nutritional content. Spinach, arugula, kale and collards are rich in vitamins A and C and are high in fiber and folate. Research has shown that regular consumption of leafy greens may lead to a slower rate of cognitive decline and improved memory as you age. Try adding these nutritional powerhouses to whole grain pasta, soups and smoothies to sneak in those extra nutritional benefits.
Nuts : Nuts like walnuts, pistachios and almonds are beneficial to your overall brain health. Almonds are known to help improve memory. Pistachios can help with inflammation and may help with cognition. Walnuts are rich in antioxidants and DHA, a fatty acid that may improve learning ability.
Taking care of your brain health also means taking care of your gut. A healthy and balanced microbiome is connected to reduced risk of various mental health disorders and improved memory and cognition. Care for your gut health by enjoying these foods.
Probiotic foods: Probiotic foods help produce a healthy microbiome which is responsible for producing chemicals like serotonin and dopamine. These compounds help regulate mood and support brain health. Probiotic foods include yogurt, kimchi, buttermilk, fermented vegetables like sauerkraut, and some cheeses. Studies have shown that regular consumption of probiotic foods is linked to reduced risk of anxiety and depression and enhances memory and learning abilities.
Prebiotic foods: Prebiotic foods such as garlic, onions, and bananas help to nourish beneficial gut bacteria, and in turn, support brain health. These foods help with the production of compounds like short chain fatty acids that play an important role in reducing inflammation to support brain function. To maintain a healthy gut and protect your brain, fuel your microbiome by eating plenty of fiber from fruits and vegetables, whole grains, and legumes like beans or chickpeas. Adults should aim for 25-30 grams per day.
Scientists capture NMDAR protein’s ‘twist’ motion, key to brain signaling
Proteins are constantly performing a kind of dance. They move and contort their bodies to fulfill specific functions inside our bodies. The NMDAR protein executes an especially hard dance routine in our brains. One wrong step can lead to a range of neurological disorders. NMDAR binds to the neurotransmitter, glutamate, and another compound, glycine . These bindings control NMDAR’s dance steps. When their routine is over, the NMDAR opens. This open ion channel generates electrical signals critical for cognitive functions like memory.
The problem is that scientists couldn’t figure out the last step in NMDAR’s routine-;until now. Cold Spring Harbor Laboratory Professor Hiro Furukawa and his team have deciphered the critical dance move in which NMDAR rotates into an open formation. In other words, they’ve learned the NMDAR “Twist.”
To capture this key step, Furukawa and his team used a technique called electron cryo-microscopy (cryo-EM), which freezes and visualizes proteins in action. First, the team had to find a way to keep a type of NMDAR called GluN1-2B in its open pose long enough to image it. So, Furukawa teamed up with Professors Stephen Traynelis and Dennis Liotta at Emory University. Together, they discovered a molecule that favors NMDAR in an open position. It’s not the most stable conformation. There are many pieces dancing independently in NMDAR. They have to coordinate with each other. Everything has to go perfectly to open the ion channel. We need a precise amount of electrical signals at the right time for proper behaviors and cognitions.” Hiro Furukawa, Professor, Cold Spring Harbor Laboratory The cryo-EM images allow researchers to see precisely how the NMDAR’s atoms move during its “Twist.” This may one day lead to drug compounds that can teach the correct moves to NMDARs that have lost a step. Better drugs that target NMDARs might have applications for neurological disorders like Alzheimer’s and depression.
“Compounds bind to pockets within proteins and are imperfect, initially. This will allow us and chemists to find a way to fill those pockets more perfectly. That would improve the potency of the drug. Also, the shape of the pocket is unique. But there could be something similarly shaped in other proteins. That would cause side effects. So, specificity is key,” Furukawa explains.
Indeed, there are many types of NMDARs in the brain. Another recent study from Furukawa’s lab offers the first view of the GluN1-3A NMDAR. Surprisingly, its dance moves are completely different. This routine results in unusual patterns of electrical signals.
In other words, we’re mastering the Twist. Next up: the headspin.
Source:
Cold Spring Harbor Laboratory
Journal references:
Chou, T.-H., et al . (2024). Molecular mechanism of ligand gating and opening of NMDA receptor. Nature . doi.org/10.1038/s41586-024-07742-0 .
Michalski, K., & Furukawa, H. (2024). Structure and function of GluN1-3A NMDA receptor excitatory glycine receptor channel. Science Advances . doi.org/10.1126/sciadv.adl5952 .
Novo’s older obesity drug shows biological effect on Alzheimer’s patients in small trial
FILE PHOTO: A view of the logo of Novo Nordisk at the company’s office in Bagsvaerd, on the outskirts of Copenhagen, Denmark, March 8, 2024. REUTERS/Tom Little/File Photo Purchase Licensing Rights, opens new tab CHICAGO/LONDON, July 30 (Reuters) – Data from a small clinical trial published on Tuesday showed that a drug from the GLP-1 receptor agonist class known for weight loss slowed the loss of brain volume in people with mild Alzheimer’s disease.
The trial results, published at the Alzheimer’s Association International Conference, provided the first glimpse of how GLP-1 drugs may act on hard-to-treat brain disorders.
The trial studied just 204 patients in Britain, half of whom received Novo Nordisk’s (NOVOb.CO), opens new tab earlier-generation GLP-1 drug liraglutide, and the other half a placebo.
The trial did not meet its primary endpoint, or main goal, which was change in the cerebral glucose metabolic rate, an assessment of brain function.
It did meet the secondary endpoints. It showed liraglutide appeared to reduce shrinking in the parts of the brain that control memory, learning, language and decision-making by nearly 50% compared to placebo.
The trial was not sponsored by Novo. However, the Danish drugmaker is testing its new-generation, more effective GLP-1 drug semaglutide — sold as diabetes drug Ozempic and obesity drug Wegovy — in thousands of patients with early Alzheimer’s. Its two trials began in 2021 and results are expected in 2025.
Rebecca Edelmeyer, senior director of scientific engagement at the Alzheimer’s Association, told Reuters in an interview that the results published on Tuesday were “really intriguing”.
“This is our first time really seeing this type of intervention readout in a clinical trial,” she said.
Researchers told Reuters last year that diabetes regimens, from Ozempic to insulin and metformin, appear to address several different aspects of the metabolic system implicated in Alzheimer’s, including a protein called amyloid and inflammation.
The hope is that improving glucose utilisation and reducing inflammation in the body – including the brain – could slow progression of Alzheimer’s.
Still, the trial published on Tuesday was not designed to measure cognitive benefits, and some scientists urged caution.
“The repurposing of drugs is an important avenue of research but there is a lot of uncertainty here,” said Stephen Evans, emeritus professor at the London School of Hygiene and Tropical Medicine.
He said the shrinking in the memory and learning parts of the brain observed in the small trial “may not translate to important cognitive benefits” and the results did not demonstrate that liraglutide could protect against dementia, though pursuing a larger trial would be worthwhile.
Reporting by Julie Steenhuysen in Chicago and Maggie Fick in London; Editing by Bernadette Baum
Purchase Licensing Rights
Maggie is a Britain-based reporter covering the European pharmaceuticals industry with a global perspective. In 2023, Maggie’s coverage of Danish drugmaker Novo Nordisk and its race to increase production of its new weight-loss drug helped the Health & Pharma team win a Reuters Journalists of the Year award in the Beat Coverage of the Year category. Since November 2023, she has also been participating in Reuters coverage related to the Israel-Hamas war. Previously based in Nairobi and Cairo for Reuters and in Lagos for the Financial Times, Maggie got her start in journalism in 2010 as a freelancer for The Associated Press in South Sudan.
Novo Nordisk’s Older Weight Loss Drug May Slow Cognitive Decline in Alzheimer’s Patients, Small Study Shows Brain-Protecting Benefits
A Phase 2b clinical trial presented at the Alzheimer’s Association International Conference (AAIC) 2024 reveals that Novo Nordisk A/S’s NVO older generation GLP-1 drug, liraglutide, may slow cognitive decline by protecting the brain.
Related: Novo Nordisk’s Ozempic Reduces Smoking-Related Health Interventions In Diabetic Patients, Study Finds .
GLP-1 (Glucagon-Like Peptide-1) drugs are a class of medications primarily used to treat type 2 diabetes and, in some cases, obesity.
GLP-1 receptor agonists mimic the natural hormone glucagon-like peptide and help manage diabetes, promote weight loss, and reduce heart disease, stroke, and kidney disease risks.
Animal studies indicate these drugs may also have neuroprotective effects, reducing early forms of amyloid and normalizing brain glucose processing.
The study included 204 patients with mild Alzheimer’s across 24 UK clinics. Participants received up to 1.8 mg of liraglutide or a daily placebo for a year.
The primary endpoint, change in cerebral glucose metabolic rate (an assessment of brain function), was not met. However, significant benefits were observed in secondary endpoints like clinical and cognitive measures and brain volume changes.
Those on liraglutide experienced almost 50% less brain volume loss in critical regions such as the frontal, temporal, and parietal lobes.
Cognitive testing before and after treatment showed an 18% slower decline in cognitive function among those on liraglutide compared to the placebo group.
Cognitive function was measured using a composite score from 18 different tests. The study also reported gastrointestinal issues, such as nausea, as the most common side effects, but serious side effects were relatively rare.
Further research is warranted, but current late-stage trials of GLP-1 analogs, like the EVOKE Plus trial of semaglutide, are well-positioned to explore these findings further.
Reuters noted that its two trials began in 2021 and results are expected in 2025.
Liraglutide, marketed as Saxenda for weight loss and Victoza for diabetes, has already been approved by the FDA.
Price Action: NVO stock is up 0.50% at $128.69 at the last check on Tuesday.
Read Next: Insulin Device Maker Embecta Weighs Sale After 70% Share Decline Following Becton Dickinson Spin-Off .
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Epigenetics Unlocks Secrets of Memory Formation
Summary: A new study reveals that the epigenetic state of neurons determines their role in memory formation. Neurons with open chromatin states are more likely to be recruited into memory traces, showing higher electrical activity during learning.
Researchers demonstrated that manipulating these epigenetic states in mice can enhance or impair learning. This discovery shifts the focus from synaptic plasticity to nuclear processes, offering potential new avenues for treating cognitive disorders.
Key Facts:
> Neurons with open chromatin states are more likely to be involved in memory formation.
Manipulating the epigenetic state of neurons in mice can enhance or impair learning.
This research shifts the focus from synaptic plasticity to nuclear processes in learning.
Source: EPFL
When we form a new memory, the brain undergoes physical and functional changes known collectively as a “memory trace”. A memory trace represents the specific patterns of activity and structural modifications of neurons that occur when a memory is formed and later recalled.
But how does the brain “decide” which neurons will be involved in a memory trace? Studies have suggested that the inherent excitability of neurons plays a role, but the currently accepted view of learning has neglected to look inside the command center of the neuron itself, its nucleus. In the nucleus, there seems to be another dimension altogether that has gone unexplored: epigenetics. A neuron can be epigenetically open when the DNA inside its nucleus is unraveled or relaxed; and closed when the DNA is compact and tight. Credit: Neuroscience News Inside every cell of a given living organism, the genetic material encoded by the DNA is the same, yet the various cells types that make up the body, like skin cells, kidney cells, or nerve cells each express a different set of genes. Epigenetics is the mechanism of how cells control such gene activity without changing the DNA sequence.
Now, scientists at EPFL led by neuroscientist Johannes Gräff have explored whether epigenetics might affect the likelihood of neurons to be selected for memory formation.
Their research on mice, now published in Science , shows that the epigenetic state of a neuron is key to its role in memory encoding.
“We are shedding light on the earliest step of memory formation from a DNA-centric level”, says Gräff.
Gräff and his team wondered if epigenetic factors could influence the “mnemonic” function of a neuron. A neuron can be epigenetically open when the DNA inside its nucleus is unraveled or relaxed; and closed when the DNA is compact and tight.
They found that it is the open ones that are more likely to be recruited into the “memory trace”, the sparse set of neurons in the brain that shows electrical activity when learning something new. Indeed, the neurons that were in a more open chromatin state were also the ones demonstrating higher electrical activity.
The EPFL scientists then used a virus to deliver epigenetic enzymes to artificially induce openness of the neurons. They found that the corresponding mice learnt much better. When the scientists used the opposite approach to close the neurons’ DNA, the mice’s ability to learn was cancelled.
The findings open up new ways to understand learning that encompass the neuron’s nucleus, and may even lead one day to medication for improving learning. As Gräff explains: “They move away from the dominant neuroscientific view on learning and memory that focuses on the importance of synaptic plasticity, and newly place emphasis on what happens inside the nucleus of a neuron, on its DNA.
“This is especially important, as many cognitive disorders such as Alzheimer’s disease and post-traumatic stress disorder are characterized by epigenetic mechanisms gone wrong.” About this memory and epigenetics research news
Author: Nik Papageorgiou
Source: EPFL
Contact: Nik Papageorgiou – EPFL
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“ Chromatin plasticity predetermines neuronal eligibility for memory trace formation ” by Johannes Gräff et al. Science
Abstract
Chromatin plasticity predetermines neuronal eligibility for memory trace formation INTRODUCTION
During development, epigenetic heterogeneity gives rise to different cell types with different functions. By stably instructing the activation and deactivation of genomic loci to catalyze specific signaling cascades, epigenetic mechanisms play a pivotal role in lineage commitment and cellular differentiation. What remains elusive, however, is whether chromatin plasticity plays an equally important role in the development of dynamic functions in fully differentiated cells, such as adult neurons.
One of the most intriguing features of neurons is their capacity for information encoding. Notably, for each new piece of information memorized the brain deploys only a subset of its neurons, implying that even within the same developmentally defined cell type, not all neurons are equally fit for information encoding at any given time. RATIONALE
The dependence of memory formation on neuronal selection made us ask whether chromatin architecture might be heterogenous enough, among otherwise seemingly homogeneous cellular identities, to drive information encoding. And specifically, whether enhanced chromatin plasticity could be a catalyst force to prime neurons to be preferentially selected for memory formation. RESULTS Focusing on the mouse lateral amygdala, a key brain region responsible for the encoding of associative forms of memory, we discovered that its excitatory neurons indeed exhibit heterogeneous chromatin plasticity, and further, that those preferentially recruited into learning-activated neurons were enriched for hyperacetylated histones, an abundant epigenetic modification in the brain.To functionally test this correlation between chromatin plasticity and information encoding, we subsequently manipulated histone acetylation levels by either increasing or decreasing histone acetyltransferases (HATs) in these neurons. We found that a gain-of-function of histone acetylation-mediated epigenetic plasticity facilitated neuronal recruitment into the memory trace whereas a loss-of-function thereof prevented memory allocation.Interested in the molecular mechanisms underlying this selection, we next performed single nucleus multiome sequencing for the simultaneous assessment of chromatin accessibility and gene expression changes occurring in the epigenetically modified neurons.These results revealed gained chromatin accessibility or increased expression at genomic locations closely related to structural and synaptic plasticity, as well as to neuronal excitability, which has been identified as an important physiological process for information encoding. Accordingly, we found that […]
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.
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