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Alzheimer's disease has been reversed in mice with a drug that replicates the benefits of exercise for the brain.
The revolutionary therapy has generated new neurons, improving the thinking abilities of laboratory animals by destroying the unwanted proteins that cause the devastating disease.
This raises the possibility of developing drugs that fuel the production of brain cells called neurogenesis.
The lead author, Professor Rudolph Tanzi, director of the Genetics and Aging Research Unit at Massachusetts General Hospital, said, "In our study, we showed that exercise was the only One of the best ways to trigger neurogenesis.
Revolutionary Massachusetts General Hospital therapy has generated new neurons, improving the thinking abilities of laboratory animals by destroying unwanted proteins that cause the devastating disease. The authors say that they firmly believe that it will be true for humans too
"Then, in determining the molecular and genetic events involved, we determined how to mimic the beneficial effects of exercise through gene therapy and pharmacological agents."
The US team hopes a similar technique could work in humans. Plans to explore this are already underway.
The lead author, Dr. Se Hoon Choi, based in the same lab, said, "Although we still can not afford the same effects in patients, we have determined the precise targets of proteins and genes. . & # 39;
Even a 30 – minute brisk walk, jog or bike ride pumps blood to the brain, providing the oxygen and nutrients it needs to function at its best.
This enhances mental functions by promoting the birth of neural progenitor cells in the hippocampus, the area of the brain that controls memory.
Experiments on adult mice genetically modified to develop symptoms similar to those of Alzheimer's disease have shown that these new neurons could be induced either by exercise or by drugs and gene therapy.
At first, only the exercise worked. Indeed, physical activity uses a protein called BDNF, known to protect brain cells.
Dr. Choi explained, "We discovered that the main difference was that exercise also resulted in the production of a neurotrophic factor derived from the brain or BDNF – known for its growth and survival – creating an environment more welcoming brain for new neurons. to survive.
"By combining drugs and gene therapy, which induced both neurogenesis and increased production of BDNF, we were able to mimic the effects of exercise on cognitive function."
In behavioral tests, animals in which neurogenesis had been induced by exercise had improved cognitive performance and reduced beta-amyloid levels.
These are the rogue proteins that form clumps in the brains of patients with Alzheimer's disease.
Mice in which it had been induced pharmacologically and genetically had limited benefits, up to the administration of BDNF.
Tanzi said, "Although exercise-induced AHN improves cognition in Alzheimer's mice by activating neurogenesis, try to achieve this result by using gene therapy and medications. not helped.
"Indeed, the newly born neurons, induced by drugs and gene therapy, were not able to survive in areas of the brain already ravaged by the pathology of Alzheimer's disease, particularly neuroinflammation. We therefore asked how exercise-induced neurogenesis differs.
The study published in Science shows that inflammation in the brain of patients with Alzheimer's disease can block these benefits.
Physical activity can "cleanse" the environment, allowing new nerve cells to survive and thrive and improve cognition in Alzheimer mice.
Tanzi added, "The lesson learned was that it is not enough to activate the birth of new nerve cells, it must simultaneously" clean "the neighborhood in which they are born to ensure the survival and development of new cells.
"Exercise can do this, but we have found ways to mimic these beneficial cognitive effects by applying drugs and gene therapy that simultaneously activate neurogenesis and BDNF production."
The researchers also found that blocking neurogenesis in young mice with Alzheimer's shortly after birth resulted in more pronounced cognitive deficits later in life.
Tanzi said, "We will then examine whether promoting neurogenesis safely in patients with Alzheimer's disease will help to alleviate the symptoms of the disease and whether it may help prevent the symptoms later.
"We are very excited to be looking for ways to implement our new discoveries to more effectively treat and prevent this terrible disease."
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