Age-related macular degeneration and cerebral amyloid angiopathy have similar pathologies from cholesterol-APOE-amyloid-β-complement mediated inflammation.

Document Type

Article

Publication Date

3-1-2026

Keywords

JMG, Humans, Cerebral Amyloid Angiopathy, Amyloid beta-Peptides, Macular Degeneration, Cholesterol, Inflammation, Apolipoproteins E, Complement System Proteins, Alzheimer Disease

JAX Source

Prog Retin Eye Res. 2026;111:101449.

ISSN

1873-1635

PMID

41708012

DOI

https://doi.org/10.1016/j.preteyeres.2026.101449

Grant

GH: (Funded in part by VCID CWOW (NS139948), and I am the Diana Davis Spencer Foundation Chair for Glaucoma research);

Abstract

Age-related macular degeneration (AMD) and Alzheimer's disease (AD) are neurodegenerative conditions that afflict millions of elderly people around the world. AMD is a progressive retinal disorder that leads to central vision loss whereas AD primarily causes cognitive decline and behavioral changes. While each disease has distinct clinical manifestations, the accumulation of extracellular amyloid-β is a common histopathologic finding. Similarly, cerebral amyloid angiopathy (CAA), a vascular condition that can exist independent or with AD, is characterized by the accumulation of amyloid-β in cerebral blood vessels. While significant investigation of the pathophysiologic links between AMD and AD has been conducted, the underlying similarities and differences in the pathobiology of AMD and CAA has not been considered. In this review, we discuss the common pathological features of these two conditions. We then discuss the similar pathobiology that involves cholesterol metabolism, apolipoprotein E, amyloid-β, and complement mediated inflammation. At the same time, we discuss key differences in their pathobiology. This discussion sheds new perspective and insights of their pathobiology.

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