Defective proteins clump into toxic plaques and tangles. Plaques of amyloid and tau tangles kill neurons, causing Alzheimer’s disease. So goes the central dogma that has ruled neuroscience since the early ’90s.
But in the last few years, as researchers have amassed large databases of brain scans and collections of donated tissue, it’s become apparent how frequently the conventional wisdom fails. By one recent estimate, about 30% of older adults have brains loaded with enough amyloid or tau to meet the criteria for an Alzheimer’s diagnosis, but no outward symptoms of dementia.
Since then, scientists have been racing to understand what makes these seemingly resilient individuals so special, with the hope of developing drugs that might one day mimic the same neuroprotective effects. On Wednesday, a team from the Massachusetts Institute of Technology reported that it found a key driver of this resilience — a family of proteins that act as a master regulator in the brain, preventing neurons from firing out of control. By boosting activity of these proteins in mice bred to have neurodegenerative disease, the researchers were able to preserve the animals’ cognitive function.
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