ArticleResearch square2026
CSF α-synuclein seed amplification assay positivity identifies a distinct soluble amyloid-β profile linked to fibrillar amyloid burden and structural neurodegeneration.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Purpose: To determine whether cerebrospinal fluid (CSF) α-synuclein seed amplification assay (SAA) positivity identifies a reproducible soluble amyloid-β (Aβ) configuration and whether its dimensions carry distinct information about downstream pathology and neurodegeneration. Methods: In ADNI, 72 participants (13 SAA-positive [SAA+]) had same-day BACE1 activity, sAPPβ, and mass-spectrometry Aβ38/Aβ40/Aβ42. T captured common Aβ38/Aβ40 variation and D42 Aβ42 depletion relative to Aβ38/Aβ40. A one-factor measurement-error model tested common-factor compatibility. The pattern was then tested in 560 participant-disjoint individuals (131 SAA+), with T and D42 reconstructed de novo, and related to amyloid PET, clinical change, whole-brain MRI, and tau PET. Results: In the proximal cohort, SAA + was associated with lower T (β=-0.549 SD, 95% CI -1.005 to -0.093), but this effect was compatible with the one-factor model (directional compatibility probability = 0.288). In the participant-disjoint cohort, SAA + was associated with lower T (β=-0.267 SD) and higher D42 (β = 0.206 SD); their direct contrast was - 0.473 SD. Higher D42 was associated with subsequent amyloid burden, faster 0-2.5-year clinical worsening, greater whole-brain loss, and subsequent tau burden; lower T independently predicted faster whole-brain loss. Conclusions: SAA positivity identifies a reproducible T-low/D42-high soluble-Aβ configuration. The preferential association of D42 with fibrillar amyloid, tau burden, and clinical worsening links the Aβ42-selective component to the AD pathological cascade, while the overall pattern points to altered post-β-cleavage APP/Aβ handling.
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.