Alzheimer's disease was reversed in mice with a medication that mimics the benefits of exercise for the brain.
The revolutionary therapy generated new neurons, improving the thinking skills of laboratory animals by destroying the rebellious proteins that cause the devastating disease.
It raises the possibility of developing drugs that promote the production of brain cells known as neurogenesis.
The lead author, Professor Rudolph Tanzi, director of the Genetics and Aging Research Unit at Massachusetts General Hospital, said: "In our study we demonstrated that exercise is one of the best ways to activate neurogenesis.
Revolutionary therapy at the Massachusetts General Hospital spawned new neurons, improving the thinking skills of laboratory animals by destroying the rebellious proteins that cause the devastating disease. The authors say they firmly believe that it will also be true for humans
"Then, upon discovering 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 UU He says they expect a similar technique to work in humans. Plans to explore this are already underway.
The lead author, Dr. Se Hoon Choi, based in the same laboratory, said: "While we still do not have the means to safely achieve the same effects on patients, we determine the precise targets of proteins and genes to develop ways to do it in the future. & # 39;
Even a quick 30-minute walk, jog or bike ride pumps extra blood to the brain, delivering the oxygen and nutrients it needs to function to its fullest.
This improves mental functions by promoting the birth of neural progenitor cells in the hippocampus, the area of the brain that controls memory.
Experiments in adult mice genetically engineered to develop symptoms similar to those in Alzheimer's showed that these new neurons could be induced by exercise or drugs and gene therapy.
At first, only the exercise worked. This is because physical activity activates a protein called BDNF that is known to protect brain cells.
Dr. Choi explained: "We discovered that the key difference was that exercise also triggered the production of brain-derived neurotrophic factor or BDNF, which is known to be important for the growth and survival of neurons, which created a more cerebral environment. hospitable for the new neurons to survive.
"By combining drugs and gene therapy that induced neurogenesis and increased BDNF production, we were able to successfully imitate the effects of exercise on cognitive function."
In behavior tests, animals in which neurogenesis had been caused by exercise had improved cognitive performance and reduced levels of amyloid beta.
These are the dishonest proteins that form in groups in the brains of Alzheimer's patients.
Mice that had been induced pharmacologically and genetically only showed limited benefits, until the administration of BDNF.
Tanzi said: "Although exercise-induced AHN improved cognition in Alzheimer's mice by activating neurogenesis, trying to achieve that result by using gene therapy and drugs did not help.
"That was because the newborn neurons, induced by drugs and gene therapy, were not able to survive in regions of the brain already devastated by Alzheimer's disease, particularly neuroinflammation, so we asked how neurogenesis differs from exercise" .
The study published in Science shows that these benefits can be blocked by inflammation in the brain of Alzheimer's patients.
Physical activity can "cleanse" the environment, allowing new nerve cells to survive and thrive and improve cognition in Alzheimer's mice.
Tanzi added: "The lesson learned was that it is not enough to activate the birth of new nerve cells, but simultaneously to clean the neighborhood where they are born to make sure that the new cells survive and thrive.
"Exercise can achieve that, but we find ways to mimic those beneficial cognitive effects through the application of medications and gene therapy that simultaneously activate neurogenesis and BDNF production."
The researchers also found that blocking neurogenesis in younger mice with Alzheimer's shortly after birth leads to more pronounced cognitive deficits later in life.
Tanzi said: "Next we will explore whether the safe promotion of neurogenesis in Alzheimer's patients will help alleviate the symptoms of the disease and if doing so in currently healthy people at a younger age can help prevent symptoms later on.
"We are very excited to now investigate ways to implement our new findings to treat and prevent this terrible disease more effectively."