Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
WSB.APP/PS1 mice develop age-dependent cerebral amyloid angiopathy, cerebrovascular dysfunction, and white matter deficits.
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Marola Olivia J, Uyar Asli, Keezer Kelly J, Chong Chie Juan Antonio K, Elk Kevin J, Cullen Abigail E, Eldridge Kierra, Persohn Scott, Kanyinda Jonathan Nyandu, Whitesell Jennifer D, Harris Julie A, Salama Paul, Walker Ashley E, Carter Gregory W, Sasner Michael, Territo Paul R, Howell Gareth R, Onos Kristen D
Аннотация
INTRODUCTION: Cerebrovascular deficits, including cerebral amyloid angiopathy (CAA), play a key role in Alzheimer's disease (AD) pathogenesis. Here, we characterize the susceptibility of the WSB/EiJ genetic context to human AD-relevant cerebrovascular phenotypes.
METHODS: CAA and parenchymal plaque analysis and in vivo neurovascular imaging were performed on WSB.APP/PS1 brains. Transcriptomics was performed on WSB.APP/PS1 and B6.APP/PS1 brains. B6 and WSB cerebrovascular reactivity was assayed ex vivo. Additional CAA and parenchymal plaque analysis was performed on WSB.APP/PS1 mice with APOE2, APOE3, or APOE4 alleles.
RESULTS: WSB.APP/PS1 brains exhibited plaque deposition, CAA, transcriptomic overlap with human AD, myelin deficits, cerebrovascular/metabolic uncoupling, and altered cerebrovascular morphology. Aged WSB vasculature retained vasoreactivity but exhibited increased stiffness. Compared to WSB.APOE2/2APP/PS1, WSB.APOE4/4APP/PS1 mice had increased CAA and plaque-associated microglial area.
DISCUSSION: These data illustrate the utility of the WSB genetic context to model CAA and uncover vascular contributions to AD.
METHODS: CAA and parenchymal plaque analysis and in vivo neurovascular imaging were performed on WSB.APP/PS1 brains. Transcriptomics was performed on WSB.APP/PS1 and B6.APP/PS1 brains. B6 and WSB cerebrovascular reactivity was assayed ex vivo. Additional CAA and parenchymal plaque analysis was performed on WSB.APP/PS1 mice with APOE2, APOE3, or APOE4 alleles.
RESULTS: WSB.APP/PS1 brains exhibited plaque deposition, CAA, transcriptomic overlap with human AD, myelin deficits, cerebrovascular/metabolic uncoupling, and altered cerebrovascular morphology. Aged WSB vasculature retained vasoreactivity but exhibited increased stiffness. Compared to WSB.APOE2/2APP/PS1, WSB.APOE4/4APP/PS1 mice had increased CAA and plaque-associated microglial area.
DISCUSSION: These data illustrate the utility of the WSB genetic context to model CAA and uncover vascular contributions to AD.