Scientists develop new method to protect brain cells in Alzheimer’s disease Nature: reducing cellular response to stress may stop the development of dementia

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Scientists at the University of California discovered that toxic protein deposits in the brain may not directly cause cell dysfunction. Neuronal damage occurs as part of the cellular stress response, which when turned off can prevent the progression of neurodegenerative diseases (including Alzheimer’s disease). Research results published In the journal Nature.

Numerous neurodegenerative diseases, including Alzheimer’s disease (a subtype of dementia) and Parkinson’s disease, are associated with the buildup of protein clumps in the brain. It is believed to be a buildup of amyloid and tau proteins that lead to the dysfunction of neurons, which are cells designed to receive, process, store and transmit information from outside.

In a new study, scientists found that neuronal dysfunction may result not from toxic protein deposits but from the body’s inability to turn off the stress response of these cells. According to the researchers, white aggregates are responsible for keeping cellular stress mechanisms constantly active.

Scientists have discovered that a protein complex called SIFI (SIlencing Factor of Integrated Stress Response) can suppress such stress responses. However, when protein aggregates accumulate, SIFI cannot perform its normal functions. The researchers suggested that the use of drugs that could remove toxic protein accumulations would allow SIFI to “function at full capacity” and reduce cellular stress levels. This type of therapy could potentially prevent the development and progression of neurodegenerative diseases.

Previous scientists closer to understanding Causes of certain social behaviors in autism.

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