A physiologic biomarker for cerebral amyloid angiopathy

Abstract

Cerebral amyloid angiopathy (CAA), a common small-vessel disease of older adults characterized by accumulation of amyloid-β in leptomeningeal and cortical blood vessels, is a well-established cause of intracerebral hemorrhage.(1) Recent years have seen the emergence of clinical research reports establishing associations between CAA, ischemic brain injury, and vascular cognitive impairment (VCI). CAA patients had a higher load of chronic microvascular white matter hyperintensities (WMH), small infarcts, as well as a high degree of WMH progression.(2,3) A more recent report showed that vascular amyloid load strongly correlated with ischemic WMH in CAA.(4.)