How to resist cognitive decline in the brain? Research discovers new treatment targets

With advances in medical and health care, the average life span of human beings has continued to increase in the past few decades

However, there is also a small group of lucky patients who can resist cognitive decline caused by age and pathological changes

Recently, the team of Professor Lihui Cai from the Massachusetts Institute of Technology found a key protein whose activity may explain how cognitive flexibility comes from

This positive result points out the direction for the development of new therapies, and related papers were recently published in Science Translational Medicine, a subsidiary of Science

This new discovery by scientists is not accidental, but is based on a phenomenon observed and proven by researchers and clinicians over the past years, that is, the more colorful the environment, the more protective the brain

In animal experiments, if the mice are allowed to live in a cage with a lot of toys and a larger space for activity, their cognitive flexibility will be better than those of mice with a monotonous living environment

▲Schematic diagram of mouse experiment: Different environments with different levels of abundance have different effects on cognitive performance (picture source: reference [1])

After a series of comparisons and analyses, a transcription factor called MEF2 emerged

▲Human data from the two cohorts show that there is a correlation between the expression of MEF2 in the prefrontal lobe of the brain and the overall cognitive function (picture source: reference [1])

Following this discovery, the researchers proposed a potential strategy to improve cognitive flexibility: increasing the activity of MEF2

Although the pathological tau protein in these mice, a characteristic pathological protein of Alzheimer’s disease, has not been eliminated, the overexpression of Mef2 gene is sufficient to protect the mice’s neurons and reduce the incidence of neurodegenerative diseases.

Note: The original text has been deleted

Reference materials:

[1] Scarlett J.