Protein May Determine Who Gets Alzheimer’s Disease by Maria Sanchez

Alzheimer’s is a type of dementia that causes problems with memory, thinking, and behavior. The symptoms of this disease usually develop slowly and worsen with time, becoming severe enough to interfere with daily tasks, such as activities that require multiple steps or even communicating with others.

Some common symptoms of this disease are increased memory loss and confusion,problems recognizing family, friends, and even oneself, continuously repeating stories, favorite words, or motions, inability to communicate, lack of control over bowel and bladder,difficulty performing tasks that have multiple steps like getting dressed, and needing help with activities of daily living.

Scientists believe Alzheimer’s disease prevents parts of a cell from running properly. Although they do not know where the trouble starts, they do know that backups and breakdowns in one system cause problems in other areas. As damage spreads, cells lose their ability to do their jobs and, eventually die, causing irreparable changes in the brain.

It has always been a mystery why some people whose brains accumulate the plaques and tangles like those associated with Alzheimer’s do not develop the disease. Research done at Harvard can shed some light as to what the answer to this mystery is.

“Why should a fetal gene be coming on in an aging brain?” questioned Dr. Bruce A. Yankner, a professor of genetics at Harvard Medical School and the lead author of the new study. He thought that this was because in aging brains, since birth, encounter great stress, threatening neurons that cannot regenerate if harmed.

New research suggests that Alzheimer’s disease and other forms of dementia may be related to a failure in the brain’s stress response system. When this system functions properly, it is capable of protecting the brain from abnormal Alzheimer’s proteins. If this system is wrecked, critical areas of the brain begin to degenerate.

It is a credible explanation as to why some people are more susceptible to Alzheimer’s than others. Scientist’s research is concentrated on a protein called REST. This protein was previously thought to act mostly in the brains of developing fetuses. It now also seems to protect neurons in healthy elderlies from aging-related stresses. But in people who suffer from Alzheimer’s or other dementias, the protein is harshly depleted in key regions of the brain.

His team discovered that REST appears to switch off genes that promote cell death, protecting neurons from normal aging processes like inflammation, energy decrease, and oxidative stress. It was found that healthy adults between the ages of 73 and 106 had a sufficient amount of REST proteins in their brains.

People with Alzheimer’s and other dementias such as mild cognitive impairment, frontotemporal dementia, and Lewy body dementia had much less REST in parts of the brain affected by these diseases than healthy brains.

This was true of people who had issues with memory. People who remained cognitively healthy but whose brains had the same buildup of tau tangles  and amyloid plaques (present in the brains of those with Alzheimer’s) had three times more strands of rest REST than those suffering from Alzheimer’s disease. The studies conducted proved that roughly a third of people who have these plaques and tangles will not progress to show symptoms of Alzheimer’s disease.

The protein could lead to the development of new drugs for dementia, which has so far been nearly impossible to treat in the past. However, this needs to be further studied to conclude that it could eventually led to effective treatment. Things such as whether the decline of REST was a cause or effect of brain deterioration still need to be determined.

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