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Updated: Jun 28, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Inflammation profiles in Alzheimer's disease relate to cognition and neurodegeneration
Katherine R Birditt1,2, Kalliopi Mavromati3, Peter Swann4
1Department of Clinical Neurosciences, University of Cambridge and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge, UK.
Introduction:
Immune signaling alterations have been implicated in Alzheimer's disease (AD) pathophysiology, but their heterogeneity across the disease continuum in real-world cohorts is poorly characterized, limiting the development of stratified immunomodulatory approaches.
Methods:
In a diverse multicenter cohort (BioHermes) of 176 amyloid-positive individuals with AD/mild cognitive impairment (MCI) and 173 age and sex-matched controls, principal component analysis was performed on Luminex-measured plasma cytokines to derive inflammatory signatures, and their direct/indirect associations with cognition and neurodegeneration.
Results:
Two components were identified. Proinflammatory Component 2 was elevated in AD/MCI and in Black/African American participants, and strongly associated with poorer cognition (independently of neurofilament light [NfL], phosphorylated tau 217 [p-tau217], and glial fibrillary acidic protein [GFAP]). Inflammatory Component 1 showed an indirect association with cognition, mediated by neurodegeneration (plasma NfL).
Discussion:
Plasma inflammation profiles were associated with poorer cognition via direct and neurodegeneration-mediated pathways, supporting their potential use as stratification markers in AD therapeutics.
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