Vicious circle of amyloid and leptomeningeal macrophages evokes vascular dysfunction in CAA
Wake, H.; Hartantyo, R. Y.; TSUJI, T.; Hou, L.; Saito, R.; Yamasaki, A.; Kochi, T.; Saito, Y.; Tada, M.; Cheung, D. L.; Moorhouse, A. J.; Prinz, M.; Masuda, T.; Kakita, A.
Show abstract
The subarachnoid space contains leptomeningeal arteries and resident immune cells known as subarachnoid macrophages (SAMs). In Alzheimers disease (AD) and related cerebral amyloid angiopathy, amyloid-{beta} (A{beta}) 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 A{beta} deposition and identified a distinct SAM population that migrates to and phagocytoses these arterial A{beta} 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 A{beta} deposition, identifying SAMs as a potential therapeutic target in AD.
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