Last week, the Harvard Medical School lab of Bruce Yankner ’76 added a key finding to the research on the causes of Alzheimer’s disease, identifying the role that a protein called REST (repressor element 1-silencing transcription factor) plays in a normal aging brain.
In studies published March 19 in the journal Nature, Yankner and his co-authors found that REST may protect the brain from stress, and that declining REST may contribute to the degeneration of neurons in the brains of those with Alzheimer’s or other cognitive impairment.
As Yankner, a professor of genetics and neurology at Harvard Medical School, told The Boston Globe, “One very positive, optimistic note from this study is that it suggests that dementia can be resisted by some people, and it provides the first molecular inklings of how that might occur.”
Could the discovery translate into therapies to prevent Alzheimer’s? MIT researchers Li-Huei Tsai and Ram Madabhushi addressed the question in a commentary piece, also published in the March 19 Nature, noting that REST can be activated by a certain type of molecular signaling. “However, such activation is also implicated in the development of various cancers, and so this approach would probably require careful targeting,” Tsai and Madabhushi wrote, adding that “a deeper understanding of the molecular mechanisms that govern REST activation in the ageing brain will be crucial for such efforts to be successful.”
Yankner, who studied biomedical sciences as an undergraduate and earned his M.D. and Ph.D at Stanford, researches the pathogenic mechanisms in several diseases, including Alzheimer’s, Down syndrome, Parkinson’s disease, and diabetes. In 2010, he received the National Institutes of Health Director’s Pioneer Award, a grant that supports his work on aging and age-related degenerative disorders.
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