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▎Editor of WuXi AppTec's content team With the advancement of medical and health care, the average life span of human beings has been increasing in the past few decades
.
At the same time, diseases caused by aging have become common, such as Alzheimer's disease
.
Most of the unfortunately suffering from Alzheimer's disease or other similar neurodegenerative diseases will experience symptoms of worsening memory, impaired cognitive function, and eventually develop dementia
.
However, there is also a small group of lucky patients who can resist cognitive decline caused by age and pathological changes
.
Although the brain shows some molecular signs specific to the disease, their actual cognitive performance is better than expected by pathological changes
.
In the words of the researchers, these patients have stronger "cognitive resilience" (cognitive resilience)
.
Image source: 123RF 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
.
In animal experiments, the researchers artificially enhanced the activity of this protein in the mouse brain, which proved to help Alzheimer's disease model mice resist cognitive decline
.
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
.
The environment here is rich, including social activities, physical activities and other diversified stimuli, which are considered to be the most effective way to activate cognitive flexibility
.
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
.
Therefore, the researchers first compared the two groups of mice with different living environments in detail to find out which molecules in their brain cells showed significant differences
.
After identifying the candidate molecule, the researchers verified it in Alzheimer's disease patients and healthy people
.
▲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
.
In mice living in a rich environment, the activity of this transcription factor in neurons is particularly high; and in patients with Alzheimer's disease whose cognitive function remains normal, many downstream genes regulated by MEF2 show enhanced expression, and The transcriptional activity of MEF2 can strongly predict the end-stage cognitive performance of patients
.
These results suggest that the activity of MEF2 may be a key factor in regulating cognitive flexibility
.
▲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 finding, the researchers proposed a way to improve recognition A potential strategy for knowing flexibility: increase the activity of MEF2
.
As a proof of concept, they overexpressed two Mef2 genes (Mef2a and Mef2c) in mice with neurodegeneration
.
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.
Common neurons are overexcited
.
More strikingly, their performance in a series of cognitive tests has also improved, indicating that the increased transcriptional activity of MEF2 plays an important role in promoting cognitive flexibility
.
The researchers concluded: "This work can guide the development of new therapies to promote cognitive health and protect the brain from damage from various neurological diseases
.
" References: [1] Scarlett J.
Barker et al.
, ( 2021) MEF2 is a key regulator of cognitive potential and confers resilience to neurodegeneration.
Science Translational Medicine.
.
At the same time, diseases caused by aging have become common, such as Alzheimer's disease
.
Most of the unfortunately suffering from Alzheimer's disease or other similar neurodegenerative diseases will experience symptoms of worsening memory, impaired cognitive function, and eventually develop dementia
.
However, there is also a small group of lucky patients who can resist cognitive decline caused by age and pathological changes
.
Although the brain shows some molecular signs specific to the disease, their actual cognitive performance is better than expected by pathological changes
.
In the words of the researchers, these patients have stronger "cognitive resilience" (cognitive resilience)
.
Image source: 123RF 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
.
In animal experiments, the researchers artificially enhanced the activity of this protein in the mouse brain, which proved to help Alzheimer's disease model mice resist cognitive decline
.
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
.
The environment here is rich, including social activities, physical activities and other diversified stimuli, which are considered to be the most effective way to activate cognitive flexibility
.
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
.
Therefore, the researchers first compared the two groups of mice with different living environments in detail to find out which molecules in their brain cells showed significant differences
.
After identifying the candidate molecule, the researchers verified it in Alzheimer's disease patients and healthy people
.
▲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
.
In mice living in a rich environment, the activity of this transcription factor in neurons is particularly high; and in patients with Alzheimer's disease whose cognitive function remains normal, many downstream genes regulated by MEF2 show enhanced expression, and The transcriptional activity of MEF2 can strongly predict the end-stage cognitive performance of patients
.
These results suggest that the activity of MEF2 may be a key factor in regulating cognitive flexibility
.
▲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 finding, the researchers proposed a way to improve recognition A potential strategy for knowing flexibility: increase the activity of MEF2
.
As a proof of concept, they overexpressed two Mef2 genes (Mef2a and Mef2c) in mice with neurodegeneration
.
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.
Common neurons are overexcited
.
More strikingly, their performance in a series of cognitive tests has also improved, indicating that the increased transcriptional activity of MEF2 plays an important role in promoting cognitive flexibility
.
The researchers concluded: "This work can guide the development of new therapies to promote cognitive health and protect the brain from damage from various neurological diseases
.
" References: [1] Scarlett J.
Barker et al.
, ( 2021) MEF2 is a key regulator of cognitive potential and confers resilience to neurodegeneration.
Science Translational Medicine.
