Affiliations: [a] Imaging Genetics Center, Mark and Mary Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, Marina Del Rey, CA, USA
| [b] Ethel Percy Andrus Gerontology Center, USC Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, USA
| [c] Department of Biomedical Engineering, Corwin D. Denney Research Center, Viterbi School of Engineering, University of Southern California, Los Angeles, CA, USA
Correspondence:
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Correspondence to: Koral V. Wheeler, Imaging Genetics Center, Mark and Mary Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, 4676 Admiralty Way, Marina Del Rey, CA 90292, USA. Tel.: +1 323 442 7246; E-mail: Koralwhe@usc.edu.
Abstract: Cerebral amyloid angiopathy (CAA) is characterized by amyloid-β aggregation in the media and adventitia of the leptomeningeal and cortical blood vessels. CAA is one of the strongest vascular contributors to Alzheimer’s disease (AD). It frequently co-occurs in AD patients, but the relationship between CAA and AD is incompletely understood. CAA may drive AD risk through damage to the neurovascular unit and accelerate parenchymal amyloid and tau deposition. Conversely, early AD may also drive CAA through cerebrovascular remodeling that impairs blood vessels from clearing amyloid-β. Sole reliance on autopsy examination to study CAA limits researchers’ ability to investigate CAA’s natural disease course and the effect of CAA on cognitive decline. Neuroimaging allows for in vivo assessment of brain function and structure and can be leveraged to investigate CAA staging and explore its associations with AD. In this review, we will discuss neuroimaging modalities that can be used to investigate markers associated with CAA that may impact AD vulnerability including hemorrhages and microbleeds, blood-brain barrier permeability disruption, reduced cerebral blood flow, amyloid and tau accumulation, white matter tract disruption, reduced cerebrovascular reactivity, and lowered brain glucose metabolism. We present possible areas for research inquiry to advance biomarker discovery and improve diagnostics.
