Body Science

Understanding dementia and Alzheimer’s Disease, through the latest developments in research.

Fetal protein may stop Alzheimer’s

Fetal protein may stop Alzheimer’s

by STEPHANIE DUTCHEN

Harvard researchers have uncovered evidence that a protein that flips genes on and off – and increases naturally as we get older – helps protect the aging brain.

A series of studies, led by Dr. Bruce A. Yankner, a professor of genetics at Harvard Medical School, concluded that the protein, called REST, can repress genes involved in Alzheimer’s.

As The New York Times reports, REST switches off  genes that cause cell death, which in turn helps to protect the brain from deterioration due to aging.

Researchers found that REST levels were low in the brains of people diagnosed with Alzheimer’s. They hope that these discoveries might one day lead new drug treatments for dementia. The studies were published March 19, in the journal Nature.

Alzheimer’s has long been associated with toxic plaques and tangles that build up in the brain. But  past research has found that some people develop these buildups without  experiencing memory loss. This week’s new discoveries bring scientists one step closer to understanding why.

According to Yankner, the answer could be related to how the brain responds to stressors. If the brain’s response system is in good shape, it may be able to protect against neurological deterioration caused by Alzheimer’s proteins. But if something goes wrong, deterioration begins.

That’s where proteins might come in. REST is an active protein during fetal brain development, which switches off before babies are born. It becomes active again naturally as we age, in order to protect against various stresses. In fact, Yankner’s team found that in aging brains, REST was the most active gene regulator. The researchers believes this is because as the brain ages, it experiences stresses that could potentially damage neurons. In birth, the human brain experiences similar stresses.

As the Times reports, Yankner’s team used brains from brain banks to draw their conclusions. They found that in younger adults aged 20 to 35, brains had low levels of REST, but brains of those ages 73 to 106 had high levels. As people got older, their REST levels grew, unless they developed dementia. Those who developed the disease had significantly less REST. As Alzheimer’s symptoms worsened, the level of REST people had in their brains dropped.

Additionally, REST levels were only depleted in those who had memory loss and cognitive deterioration. People who maintained the same level of cognitive function, but accumulated plaques and tangles on their brains, still had three times more REST than those with symptoms of Alzheimer’s.

Researchers caution that their work is still in its early phases, and that much more needs to be done before beginning to develop a drug-based cure in humans. So far, for example,  it’s impossible to test REST levels  in living subjects.

Researchers have also yet to determine whether REST is a cause or effect of brain deterioration. Even more importantly, they’re unsure whether the protein is specific enough to neurological diseases to be able to lead to successful treatment.

For more information, read the New York Times’s coverage here, or the Boston Globe’s coverage here.



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