Researchers at Mount Sinai found that the Alzheimer's risk gene APOE4 causes pericytes, the cells that stabilize brain capillaries, to transform into scar-producing cells. This vascular fibrosis encourages amyloid buildup around blood vessels. Testing on aged mice showed that blocking TGF-beta signaling reversed the damage and restored pericyte coverage.
Treating vascular decay as a driver of Alzheimer's rather than a byproduct opens a promising avenue for prevention. Still, moving from lab-grown stem cell models and mice to human treatments is a long path with many hurdles ahead. It remains to be seen whether clearing this specific scar tissue halts cognitive decline in actual patients.
more: https://www.sciencedaily.com/releases/2026/09/260930225450.htm
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