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Imitating the effects of the exercise with drugs would help stop the Alzheimer’s

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Scientists have been verified that the practice of physical exercise has a positive effect on the brain and can prevent cognitive deterioration or slow the advance of Alzheimer’s and other similar disorders. However, many people who already suffer from this disease have mobility problems that prevent them from performing physical activity. Therefore, a team of researchers from the Cardiovascular Research Center of Massachusetts General Hospital and the Harvard Medicine School has sought an alternative that allows the same benefits to be able to step on a gym.

“We know that the exercise has many benefits for the brain and prevents Alzheimer’s disease,” said the main author, Christiane Wrann, an attached professor of Medicine at the Cardiovascular Research Center of the General Hospital of Massachusetts and Harvard’s Faculty of Medicine in a note published by the center. “Instead of prescribing exercise, we seek to activate these molecular routes through pharmacology to improve cognitive function in these patients.”

Alzheimer’s is the most common cause of dementia and in Spain affects around 800,000 people, according to data from the Spanish Society of Neurology (SEN), while, in the United States, the centers for the control and prevention of diseases (CDC) estimate that 6.7 adults live with this disease and this figure could be doubled by 2060. That is why it is so necessary to find effective options to prevent or delay their appearance.

Gene therapies or drugs that imitate the impact of exercise on the brain

Numerous studies have shown that resistance exercise – such as walking – can slow down cognitive deterioration. For example, a 2022 investigation revealed that walking about 4,000 daily steps reduces the risk of developing Alzheimer’s, and that taking 10,000 steps per day can decrease it up to 50%, Wrann stands out.

But not all patients are able to achieve that level of activity, since both the fragility of age, and the symptoms of the disease hinder the movement, recognizes the expert. “I always recommend those who can exercise it.” “There is a large population of patients who simply do not have the ability to exercise enough to obtain all these benefits,” he adds.

Therefore, Wrann’s team set out to study what happens exactly in the brain when we exercise, in order to imitate its effects. Using a technique called RNA sequencing in individual nuclei, they analyzed tissues of the hippocampus – a key region of the brain involved in memory and learning, and which is affected in the early stages of the Alzheimer’s -, taken from mice subjected to aerobic exercise (running at wheel).

This technology allows you to observe which genes are active in each brain cell. Thus, scientists can see how neurons communicate with each other and how each one reacts to the exercise, both in healthy brains, and in those with signs of Alzheéimer. The results obtained in mice were then compared with data from human brain tissues. “We know which cell communicates with the others and what they say,” said Wrann. “And we know what happens in a person’s brain with Alzheimer’s. And we also know What happens to the brain of a person with Alzheimer’s when he exercises”.

“We know with certainty that staying active delays the disease. Physically active persons have less risk of dementia or, if they develop it, they do it later”

The study results have been published in Nature neuroscience And one of the most relevant findings was the identification of the ATPPIF1 gene, whose activity seems to be related to greater neuroplasticity – That is, the ability of the brain to generate new neurons and synaptic connections – which is fundamental for learning and memory. “In Alzheimer’s, this gene becomes less active,” says Wrann. “But with the exercise, its function is reactivated. And that helps the neurons survive, regenerate and communicate better.”

The next step, according to Wrann, is to explore ways to activate this gene in humans without the need for physical exercise. The idea is to develop gene therapies or drugs that imitate the impact of exercise on the brain. “Today, biomedical science has multiple tools to modify genetic activity,” he says. “We are working to identify what would be the best way to stimulate this gene and what kind of medication could be used in people.”

Although there is still no cure for Alzheimer’s, this line of research opens new doors to delay its appearance or relieve its effects. Wrann concludes with a clear message: “What we know with certainty is that staying active delays the disease. Physically active persons have less risk of dementia or, if they develop it, they do it later. But when the deterioration is already advanced, even participating in an exercise program becomes very complicated.”


Source: www.webconsultas.com


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