ArticleNature communications2025
Two-step detection of Lewy body pathology via smell-function testing and CSF α-synuclein seed amplification.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
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Who cites it
5 citing papers in PubMed.
- Diffusion MRI and α-Synuclein Seed Amplification Status in Parkinson's Disease.Annals of neurology · 2026Article
- Biomarkers stewardship in parkinsonism: integrating alpha-synuclein seed amplification assays and neurofilament light chain into diagnostic pathways and patient communication.Journal of neurology · 2026Review
- Alzheimer's disease and cerebrovascular biomarkers in relation to odor identification in a naturalistic clinical cohort.Alzheimer's research & therapy · 2026Article
- Clinical correlates of a negative cerebrospinal fluid α-synuclein seed amplification assay result in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Cerebrospinal fluid (CSF) α-synuclein (α-syn) seed amplification assays (SAAs) can detect Lewy body pathology (LBP) with high accuracy but are invasive and costly. To address these challenges, this study evaluated a two-step workflow combining prescreening via smell-function testing with confirmatory CSF α-syn SAA testing only in individuals with reduced smell, for predicting postmortem LBP status. Among 358 autopsied participants, the two-step workflow predicted brain LBP with high accuracy overall (94%), and within clinical subgroups (clinical parkinsonism=95%; clinical Alzheimer's disease [AD]=94%; clinically unimpaired [CU]=93%). It reduced the need for confirmatory CSF testing by 43% overall (23% clinical parkinsonism; 35% clinical AD; 80% CU). In an independent in vivo cohort (N=1209), the workflow predicted CSF α-syn SAA status with 79% accuracy and reduced CSF testing by 26%. This approach may reduce invasive CSF testing, alleviating patient burden and lowering healthcare costs.
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Registered trials
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