Cellular Stress May Prevent Alzheimer’s Disease

By on April 3, 2014
BRAIN_Nerve-cell-turning-on-memory-gene-web

A study published online in Nature suggests that cellular stress can lead brain cells to produce a protein that prevents the development of Alzheimer’s disease.

Alzheimer’s disease is a form of dementia that manifests as progressive memory loss. This illness affects approximately 44.4 million people worldwide, most of whom are over the age of 65. The exact cause of Alzheimer’s is currently unknown, but it has been linked to the accumulation of amyloid β and τ proteins.

However, previous studies have found that some elderly people without any form of dementia have amyloid β and τ proteins, indicating that the amyloid proteins alone are not the cause of the symptoms of Alzheimer’s.

The most recent protein of interest is repressor element 1-silencing transcription factor (REST), a protein that turns genes on and off. REST was thought to only be present in fetal brains, where it controls gene activity during fetal brain development. This was proven to be untrue when Bruce Yankner, a neurologist at Harvard Medical School, discovered that REST levels start to increase during an individual’s thirties.

Cellular stress leads to an increase in REST in the brain. The protein turns off genes that direct cell death, resulting in brain cells remaining alive when they would normally undergo apoptosis, or cell death. Typically, brain cells cannot regenerate as other cells can. Thus, increasing levels of REST may result in a brain that functions properly for a longer period of time, because fewer cells die.

Furthermore, Yankner found that any form of cellular stress will increase the amount of REST in the brain. Some examples of cellular stress are immune reactions and protein accumulation. As people age, cellular stressors become more common, which explains the increase of REST seen in the thirties.

Adding REST can even stop neuronal death. Yankner and his colleagues added REST to mice that lacked REST. The neurons that had been dying as the mice aged stopped dying after REST was added. Even worms, specifically caenorhabditis elegans, that the worm version of REST have faster neuronal death than other worms with REST.

Yankner and his team measured REST levels in brains of elderly people that had died of Alzheimer’s. They found that REST levels were three times lower in these brains as compared to brains of people the same age without dementia. REST seems to be a protective mechanism of the brain that is compromised in individuals with Alzheimer’s or any form of dementia.

The team of scientists have already identified drugs that are capable of increasing REST levels. They are still trying to find a way to test REST levels in the blood, so that living people can be tested for dementia.

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