Abstract #0186

Impaired cerebrovascular reactivity is associated with vascular smooth muscle cell loss in a mouse model of Alzheimer’s disease

Xiuli Yang¹, Minmin Yao², Yuguo Li^1,3, Hanzhang Lu^1,3, Wenzhen Duan², and Zhiliang Wei^1,3

¹Department of Radiology, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ²Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ³The F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, United States

Synopsis

Keywords: Alzheimer's Disease, Alzheimer's Disease, vascular elasticity

Motivation: Mixed etiology involving AD and vascular issues is a common finding in clinics. However, the underlying mechanism of vascular dysfunction in AD remained to be fully understood.

Goal(s): We aim to examine cerebrovascular reactivity (CVR) in an AD model and explore biological underpinnings with histology.

Approach: CVR was assessed by a hypercapnia challenge with phase-contrast (PC) and arterial-spin-labeling (ASL) MRI in 9-month-old 5xFAD mice. Immunofluorescent staining was performed to examine amyloid-plaque deposits and vascular-smooth-muscle-cell (VSMC) densities.

Results: 5xFAD mice exhibit impaired CVR in the hippocampus, which is associated with microhemorrhage and VSMC loss. Parenchymal amyloid plaque deposits alone are insufficient to jeopardize CVR.

Impact: Impaired cerebral vascular reactivity (CVR) is associated with the loss of vascular smooth muscle cells in the hippocampus of 5xFAD model at 9 months of age.

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