Along with symptoms of cognitive decline, Alzheimer’s disease patients often have an accumulation of plaques and tangles of proteins in parts of their brains. But a long-standing question in neurology is why some elderly people develop dementia and others do not. Researchers are also left to wonder why some people have Alzheimer’s disease-like brain pathology yet show no cognitive symptoms.
A study published March 19 in Nature provides new clues that could help solve both puzzles, showing that a previously unknown stress response kicks in later in life to protect aging neurons. Researchers at Harvard Medical School found that a protein called REST, which is well characterized as a transcription factor that represses neuron-specific genes during embryogenesis, is switched on during middle- and late-adulthood, helping to protect neurons of the hippocampus and cortex from oxidative stress and the aggregated and misfolded proteins characteristic of Alzheimer’s and other neurodegenerative diseases.
“This work establishes REST as a regulator protein we have to pay a lot of attention to in the context of neurodegeneration,” said Susan Lindquist, a molecular biologist at the MIT Whitehead Institute for Biomedical Research, who was not involved in the study.
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