ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Apolipoprotein E ε4 homozygosity exacerbates retinal and cerebral microvascular dysfunction in Alzheimer's disease: A mediation analysis of vascular contributions to cognitive decline.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Retinal Microvascular Dysfunction Reflects Vascular and Alzheimer's-Related Pathology in Dementia With Lewy Bodies.CNS neuroscience & therapeutics · 2026Article
- Occupational dust exposure and cerebral small vessel disease: a public health perspective on prevention and early detection.Frontiers in medicine · 2026Review
- Retinal microvascular alterations reflect cerebral small vessel disease burden in frontotemporal dementia: a multimodal OCTA-MRI Study.Alzheimer's research & therapy · 2025Article
- Apolipoprotein E ε4 homozygosity exacerbates retinal and cerebral microvascular dysfunction in Alzheimer's disease: A mediation analysis of vascular contributions to cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
introductionApolipoprotein E (APOE) ε4 is the strongest genetic risk factor for Alzheimer's disease (AD), with homozygous carriers (ε4/ε4) experiencing accelerated cognitive decline. While its role in amyloid and tau pathology is established, its impact on retinal and cerebral microvasculature remains underexplored.
methodsA total of 107 AD (46 non-carriers, 42 heterozygotes, 19 homozygotes) underwent optical coherence tomography angiography (OCTA) to assess retinal microvasculature and magnetic resonance imaging (MRI) -derived peak width of skeletonized mean diffusivity (PSMD) to evaluate cerebral small vessel disease. Plasma biomarkers (Aβ
resultsHomozygous APOE ε4 carriers exhibited the most severe reduction in retinal microvascular density and higher PSMD (p < 0.001). Superficial retinal vessels and PSMD partially mediated APOE ε4's association with cognitive impairment. DISCUSSION: APOE ε4 homozygosity exacerbates retinal and cerebral microvascular dysfunction, which partially mediates cognitive impairment in AD. HIGHLIGHTS: Apolipoprotein E (APOE) ε4 homozygosity is associated with the most severe reductions in retinal microvascular densities and elevated cerebral small vessel disease (peak width of skeletonized mean diffusivity [PSMD]) in Alzheimer's disease (AD). Vascular dysfunction (retinal and cerebral) correlates with lower Aβ42, higher p-tau217/Aβ
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