ArticleNeurology2025
CSF α-Synuclein Seed Amplification Assays and Alzheimer Disease Biomarkers in Dementia With Lewy Bodies: Presentation and Progression.
Article in Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Alpha-synuclein co-pathology amplifies amyloid-driven tau accumulation across Braak stages without modifying tau-cognition associations.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
Abstract
BACKGROUND AND
objectivesα-Synuclein (αSyn) seed amplification assays (SAAs) accurately detect αSyn pathology in dementia with Lewy bodies (DLB). Alzheimer disease (AD) copathology occurs in ∼70% of patients with DLB at autopsy. The association of different αSyn-SAA and AD biomarker profiles with clinical outcomes in DLB can aid prognostication and inform clinical trial design.
methodsThis is a cross-sectional study of participants in the DLB Consortium (DLBC) study. The DLBC is a multicentered prospective longitudinal cohort study with participants recruited at tertiary care centers in the United States. CSF samples obtained within 1 year of baseline assessments were analyzed using αSyn-SAA and for β-amyloid (Aβ) 42/40, phosphorylated tau (p-tau) 181, and total tau (t-tau). Comparisons of baseline prevalence and degree of core DLB features, cognitive impairment, and hyposmia in participants with different CSF profiles were performed (AD-: normal Aβ42/40, p-tau181, and t-tau. AD+: Aβ42/40 abnormal, ±p-tau181, ±t-tau. Other non-AD: normal Aβ42/40 but elevated p-tau181 or t-tau levels). Longitudinal cognitive and motor declines were assessed in participants with different CSF profiles using linear mixed-effects models.
resultsNinety-nine participants had CSF αSyn-SAA and AD biomarkers available for analysis (mean age 69.8 ± 6.6, 15% female); 68% (67/99) were αSyn-SAA+. αSyn-SAA+ participants had lower baseline Montreal Cognitive Assessment (MoCA) scores (19.0 ± 5.8 vs 21.6 ± 4.7, DISCUSSION: In this well-characterized cohort of participants with clinically diagnosed DLB, αSyn-SAA positivity is associated with greater motor decline. AD copathology is common and confers additional risk of cognitive and functional decline.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.