| Aβ40 predominance | While Aβ42 is more aggregation-prone and found in parenchymal plaques, Aβ40 is the predominant isoform in CAA due to its higher affinity for cerebral blood vessel walls[@herzig2007] |
| APOE4 association | The APOE ε4 allele strongly increases CAA risk and severity |
| Vascular localization | Amyloid deposits are found primarily in the: |
| Cytoplasmic vacuolization | Early indicator of Aβ-induced injury |
| Nuclear pyknosis | Evidence of apoptotic cell death |
| Complete cell loss | Advanced CAA shows near-complete VSMC replacement by amyloid |
| Media thinning | Vessel wall thickness increases while smooth muscle content decreases[@weller2015] |
| Contractile dysfunction | Loss of contractile phenotype, transitioning to synthetic state |
| Impaired autoregulation | Reduced ability to maintain constant cerebral blood flow |
| Dysregulated matrix maintenance | Altered production of extracellular matrix proteins |
| Endothelial decoupling | Loss of endothelial-VSMC signaling coordination[@blair2021] |
| Direct pericyte binding | Aβ peptides bind to pericyte surface receptors including CD36 and RAGE |
| Databases | OMIMOrphanetClinicalTrialsPubMed |
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