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Alzheimer's blood vessel damage mechanism found
Scientific research has shown that the APOE4 genetic variant, the strongest hereditary factor for Alzheimer's disease, actively causes damage to blood vessels in the brain and promotes the accumulation of harmful proteins—not just as a consequence of the disease. Two studies confirmed that APOE4 transforms supporting cells into scar-forming cells, which enhances fibrosis and impairs blood flow through the vessels. This fibrosis can be reversed by targeting the TGF-β pathway, opening new therapeutic possibilities. Additionally, studies revealed that APOE4 leads to cholesterol buildup in astrocytes, disrupting waste clearance systems and increasing the accumulation of the harmful protein alpha-synuclein. Targeting cholesterol metabolism and lysosomal functions emerges as a promising approach for treating the disease.
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