ArticleAlzheimer's & dementia (Amsterdam, Netherlands)
Parallel neuroinflammatory pathways to cerebrovascular burden and amyloid beta in Alzheimer's disease.
Article in Alzheimer's & dementia (Amsterdam, Netherlands). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Beyond amyloid: Contributions of neuroinflammation, cerebrovascular disease, and neurodegeneration to memory impairment in the oldest-old, the LifeAfter90 Study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
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Authors and funding
19 authors.
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Abstract
introductionUpstream neuroinflammation plays an important role in Alzheimer's disease (AD) but remains poorly understood. We tested whether two distinct neuroinflammatory markers are associated with cerebrovascular burden and amyloid beta (Aβ), and downstream, with plasma phosphorylated tau (p-tau217), medial temporal lobe (MTL) cortical and hippocampal atrophy, and memory deficits.
methodsCognitively unimpaired older adults without dementia or mild cognitive impairment were recruited from a community sample (Biomarker Exploration in Aging, Cognition, and Neurodegeneration; [BEACoN];
resultsHigher plasma YKL-40 was associated with greater white matter hyperintensity (WMH), whereas higher plasma GFAP was related to increased 18F-florbetapir (FBP) standardized uptake value ratio (SUVR). Higher plasma GFAP, WMH, and FBP SUVR were independently associated with increased p-tau217. Plasma p-tau217 was associated with reduced MTL cortical thickness and hippocampal volume. Reduced hippocampal volume was related to worse memory. DISCUSSION: Future work can further investigate these neuroinflammatory pathways as potential therapeutic targets for AD.
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