ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Alpha-synuclein co-pathology in Down syndrome-associated 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 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Plasma p-tau as a biomarker for the differential diagnosis of Alzheimer's disease: a systematic review and meta-analysis.Alzheimer's research & therapy · 2026Pooled it
- Frequency of mixed neuropathologies in individuals with down syndrome with and without Alzheimer's dementia.Acta neuropathologica · 2026Article
- Amyloid-linked versus age-driven copathologies in Alzheimer's dementia: differential associations withResearch square · 2026Article
- From clinical phenotypes to molecular stratification: early differential diagnosis of four-repeat tauopathies.Frontiers in aging neuroscience · 2026Review
- The Down Alzheimer Barcelona Neuroimaging Initiative (DABNI) and its contributions to understanding Alzheimer's disease in Down syndrome: A decade of discovery.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Alpha-synuclein co-pathology in Down syndrome-associated Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
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30 authors.
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Abstract
introductionAlpha-synuclein (αSyn) seed amplification assay (SAA) enables in vivo study of αSyn but remains underexplored in Down syndrome-associated Alzheimer's disease (DSAD).
methodsWe analyzed αSyn-SAA in cerebrospinal fluid (CSF) from 270 adults with Down syndrome, from the Down Alzheimer Barcelona Neuroimaging Initiative and from the AD21 cohort from the Department of Neurology at the University Hospital, Ludwig Maximilian University of Munich, Germany. Neuropathological examinations were conducted in 19 brain donors (five with ante mortem CSF). Participants were classified as asymptomatic or symptomatic (prodromal/dementia) Alzheimer's disease (AD). CSF Aβ1-42/1-40, CSF and plasma p-Tau181, and neurofilament light chain (NfL) levels were measured. Neuropathological evaluations assessed AD neuropathological changes and Lewy body pathology (LBP).
resultsΑSyn-SAA was positive in 9.2% of cases, independent of age or cognitive status. Symptomatic αSyn-positive cases exhibited higher plasma NfL levels than αSyn-negative cases (31 vs 21 pg/mL, p = 0.027). LBP was observed in 47% of necropsies. The individual with severe neocortical LBP was αSyn-SAA-positive. DISCUSSION: These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition. HIGHLIGHTS: αSyn-SAA positivity in DSAD is 9.2%, similar to ADAD but lower than sporadic AD. Misfolded αSyn was detectable from early ages in individuals with DS. Positivity rates did not vary with age or clinical status in DS. Plasma NfL levels are higher in symptomatic αSyn-SAA positive versus negative cases. CSF αSyn seeding activity was associated with high neocortical LBP at necropsy.
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