Dysregulated microvascular reactivity in hippocampus and cortex in CVN Alzheimer's disease mouse model.

This article investigates neurovascular coupling (NVC) dysfunction in the CVN mouse model of Alzheimer's disease (AD), focusing on microvascular reactivity in acute cortical and hippocampal brain slices and hippocampal synaptic-evoked cerebral blood flow (CBF) in vivo. The study demonstrates that while young CVN mice exhibit normal capillary vasodilation in response to glutamate, NMDA, and adenosine, middle-aged and aged CVN mice show significant impairments in these vasodilatory responses alongside enhanced vasoconstriction to endothelin-1 (ET-1). Correspondingly, in vivo hippocampal CBF responses to synaptic stimulation are markedly reduced in middle-aged CVN mice compared to wild-type controls. These findings suggest that progressive, age-related microvascular dysfunction in the CVN model contributes to impaired NVC and cerebral hypoperfusion, potentially exacerbating metabolic insufficiency and AD pathology.