Vicious circle of amyloid and leptomeningeal macrophages evokes vascular dysfunction in CAA

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ABSTRACT The subarachnoid space contains leptomeningeal arteries and resident immune cells known as subarachnoid macrophages (SAMs). In Alzheimer’s disease (AD) and related cerebral amyloid angiopathy, amyloid-β (Aβ) frequently accumulates around the leptomeningeal arteries. Nevertheless, the local immune responses and their functional consequences remain poorly understood. Using longitudinal intravital imaging in a mouse model of AD, we tracked Aβ deposition and identified a distinct SAM population that migrates to and phagocytoses these arterial Aβ deposits. SAM recruitment correlated with vascular remodeling, including smooth muscle loss, aneurysm formation, and reduced cerebral perfusion. Transcriptomic profiling revealed a distinct SAM population in AD with upregulated CD39 expression. Pharmacological inhibition of CD39 attenuated arterial Aβ deposition, identifying SAMs as a potential therapeutic target in AD.

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