Breakthrough research shows that age-related decline in cognitive function can be reversible

A groundbreaking study by a team of neurologists at Stanford University leads to inflammatory hyperdrive, where immune cells become dysfunctional with age and play a role in most age-related diseases, from cancer to cognitive decline. Claims to have found. Preliminary studies suggest that this immune dysfunction may be reversed, suggesting attractive anti-aging therapies in the future.

As we grow older, our immune system slowly becomes dysfunctional. Some mean that the immune system can slow down its response to infection, while defective immune cells begin to consistently attack healthy cells, causing chronic, mild inflammation. There is also something that means. Some researchers hypothesize that this chronic inflammation plays a major role in many age-related diseases, especially the brain.

Therefore, this new study began with some general questions. What is the cause of this age-related immune dysfunction? Is this chronic inflammatory activity involved in age-related cognitive decline? And perhaps most importantly, can this mechanism be slowed down or reversed?

Specific focus of new research published in the journal NatureWas a hormone called prostaglandin E2 (PGE2). It was previously discovered that levels of this particular hormone increase with age. PGE2 is also known to promote the inflammatory activity of immune cells.

The first part of the study revealed exactly how PGE2 initiates inflammatory activity in macrophages, the basic immune leukocytes. Throughout animal and in vitro human cell studies, researchers have unveiled a series of comprehensive events showing how PGE2 directly induces inflammatory activity in macrophage dysfunction.

Researchers then confirmed that older macrophages produced significantly more PGE2 than younger macrophages in both mouse and human cells. In addition, these aged macrophages show a higher number of surfaces on the EP2 receptor, which is a receptor that binds to PGE2.

Katrin Andreason, senior author of the new study, calls this age-related inflammatory mechanism a “double pain-positive feedback loop.”

In the final part of the study, we investigated what happens when this PGE2-EP2 mechanism is blocked. Initial in vitro experiments revealed that old macrophage cells were transformed when this mechanism was disrupted. The inflammatory properties have disappeared and the old cells have been effectively rejuvenated.

Inhibition of this mechanism in an aged mouse model of cognitive decline gave even more impressive results. Older mice that received an drug that blocked PGE2-EP2 binding showed a reversal of cognitive decline and eventually functioned similarly to young mice throughout the series of cognitive tests.

Andreason suggests that this mechanism of regulating the immune system can essentially “age the brain.” Improved cognition and reduced neuroinflammation were detected even when PGE2-EP2 binding was isolated into extracerebral cells using compounds that could not cross the blood-brain barrier.

Researchers who are not involved in new research Various explanations Innovative research that is “well done,” “intriguing,” and “important.” However, they also suggest that it is a very preliminary finding and needs to be validated in humans before it can be considered close to anti-aging or anti-dementia treatment.

“This study is important because it shows that mice can reverse age-related memory loss,” explains Tara Spires Jones of the University of Edinburgh. And more work needs to be done to determine if the same effect is possible for people. “

It is clear that Andreason is looking at a long future research path. For example, the drug used in the study to block PGE2-EP2 binding is completely unprepared for clinical use in humans. In fact, Andreason suggests that they may not even be safe for humans.

Instead, this study provides researchers with new directions for developing new compounds that may disrupt the age-related inflammatory activity of this dysfunction. It may take a long time for these discoveries to lead to concrete anti-aging clinical therapies, but if verified, these underlying findings can combat a wide range of age-related diseases. It provides an exciting roadmap for creating.

“Our study suggests that cognitive aging is not a static or irreversible condition, but can be undone by reprogramming myeloid glucose metabolism to restore youthful immune function. “The researchers conclude in a new study.

New study published in journal Nature..

Source: Stanford University