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Amyloid β alters vascular CaV1.2 channel spatiotemporal properties.


ABSTRACT: A hallmark of Alzheimer's disease is reduced cerebral blood flow, which appears to occur early in disease progression and has been associated with amyloid β (Aβ) accumulation. Cerebral artery diameter is regulated by calcium influx via voltage-gated L-type CaV1.2 channels, which contribute to arterial myocyte contractility. The potential effects of Aβ on vascular CaV1.2 channels remain unclear. To address this knowledge gap, we test the hypothesis that Aβ alters vascular CaV1.2 channel spatiotemporal properties. Using freshly dissected cerebral arteries and arterial myocytes from wild-type (WT) mice, super-resolution imaging revealed that Aβ1-42, but not Aβ1-40, increased the clustering of CaV1.2 channels in male but not fem

SUBMITTER: Taylor JL 

PROVIDER: S-EPMC12857231 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature