(Natural News) The findings of a recent animal study may offer new hope to millions of people who have Alzheimer’s disease. The Harvard-led effort reports that physical exercise could improve the condition of the brains of mice with dementia.
The study shows that working out made it possible for new neurons to grow in the hippocampus, the region of the brain that handles learning and memory. The growth of new nerve cells improved the cognitive function of the brain.
Based on these results, substances that improve the hippocampus could help restore the health and function of the brain in human patients with Alzheimer’s disease. Such compounds work by enhancing the growth and survival of neurons.
The brain of an Alzheimer’s patient contains amyloid plaques and neurofibrillary tangles. These toxic structures cause severe loss of neurons and neuronal connections. The damage to brain cells is associated with the loss of memory and other symptoms of degenerating cognitive function.
Earlier experiments tried to recover brain function by taking out these plaques and tangles. The failure of these trials drove researchers to reconsider the amyloid hypothesis that supposedly explained the pathology of Alzheimer’s disease. (Related: Physical exercise reduces severity of Alzheimer’s symptoms.)
Other studies show that physical activity improved the symptoms of Alzheimer’s disease. Working out triggered biochemical alterations that improved the environment of the brain, which made it easier to grow and repair nerve cells.
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Furthermore, physical exercise activated adult hippocampal neurogenesis. During this process, neurons grew and formed connections with other brain cells at a better rate, thereby improving cognitive functions that were affected by Alzheimer’s disease.
Researchers from Harvard Medical School led an investigation of the effects of physical exercise on the growth of nerve cells in the hippocampus. They sought to determine the possibility of using these effects as therapy for patients with Alzheimer’s disease.
Their mouse model showed that exercised animals displayed higher levels of adult hippocampal neurogenesis and BDNF, a molecule that encourages the growth of neurons. These mice displayed much better memory in comparison to sedentary counterparts.
Next, the researchers reproduced the memory-improving effects of physical exercise through artificial means. They demonstrated how genetic and pharmacological techniques could improve the growth of hippocampal cells in the brains of mice with Alzheimer’s disease.
The Harvard-led joint research team also experimented with preventing hippocampal neurogenesis in animals with Alzheimer’s disease. The health of the nerve cells deteriorated in later stages, which degraded the hippocampus and impaired memory.
The study presented pre-clinical evidence that therapeutic approaches which improve hippocampal neurogenesis and raise BNDF levels could alleviate the symptoms of Alzheimer’s disease. Such treatments might even prevent dementia from appearing in the first place.
Furthermore, the researchers discovered that there was no need to get rid of amyloid plaques to improve memory functions. The discovery indicated that the amyloid hypothesis might be flawed or even incorrect.
The hypothesis holds that the accumulation of amyloid plaques is responsible for the onset of Alzheimer’s disease. However, these plaques are also present in the brains of healthy people.
If validated by future research, the Harvard study could serve as the foundation for a new and more accurate theory about the pathology of Alzheimer’s disease. Such a concept would revolve around improving the environment of the brain so that adult hippocampal neurogenesis could take place.
In the meantime, instead of waiting for a therapeutic approach that replicates the beneficial effects of exercise, patients with Alzheimer’s disease and other forms of dementia can take up an actual exercise regimen.