ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Distinct inflammatory profiles in young-onset versus late-onset Alzheimer's disease.
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 3 papers.
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Who cites it
3 citing papers in PubMed.
- Investigating causal associations among inflammatory proteins, blood metabolites, and Alzheimer's disease risk.BMC psychiatry · 2026Article
- Association between multimorbidity and young-onset dementia: a prospective study.BMC public health · 2025Article
- Distinct inflammatory profiles in young-onset versus late-onset Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
introductionNeuroinflammation, a key player in Alzheimer's disease (AD) pathogenesis, may be differentially involved in young-onset (YOAD) compared to late-onset (LOAD) AD.
methodsUsing proximity extension assay technology, we examined 737 inflammatory markers in the CSF of 26 healthy controls (63.9 ± 8.7; 12♀), 57 patients with YOAD (60.8 ± 4.9 y/o; 40♀), and 33 with LOAD (76.6 ± 4.5 y/o; 18♀). We also assessed biomarkers of AD pathology (Aβ42, p-tau181, t-tau) and neurodegeneration (neurofilament light-chain [NfL]).
resultsCompared to controls, SCRN1 and MMP10 were increased in LOAD and YOAD, but 16 markers showed YOAD-specific increases. Forty-six markers were significantly associated with NfL. P-tau181 and t-tau mediated the association between inflammatory markers and NfL in YOAD. In LOAD we could not identify a direct or indirect relationship between neuroinflammation and neurodegeneration. DISCUSSION: Using a proteomics approach, we observed an exacerbation of neuroinflammatory changes and a differential contribution of neuroinflammation to AD pathology and neurodegeneration in YOAD compared to LOAD. HIGHLIGHTS: Olink's Proximity Extension Assay was used to compare the inflammatory profile of 26 healthy controls and 90 Alzheimer's disease (AD) patients. AD patients were further stratified into young-onset (YOAD, n = 57) and late-onset (LOAD, n = 33) AD. Cerebrospinal fluid (CSF) levels of MMP10 and SCRN1 were increased in both YOAD and LOAD, but 16 proteins were only increased in YOAD. Tau mediated the association between inflammatory markers and neurodegeneration in YOAD. Neuroinflammation may be differentially involved in the pathogenesis of YOAD compared to LOAD.
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