ArticlebioRxiv : the preprint server for biology2026
Alpha-synuclein co-pathology amplifies amyloid-driven tau accumulation across Braak stages without modifying tau-cognition associations.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionAlpha-synuclein (αSyn) is the most common co-pathology in Alzheimer's disease (AD), yet its role within the amyloid-tau-neurodegeneration (ATN) cascade is unknown.
methodsWe analyzed 636 ADNI participants with CSF αSyn seed amplification assay, amyloid PET, regional tau PET (Braak I-VI), structural MRI, and cognitive composites. Interaction models tested whether αSyn modifies the amyloid-tau and tau-cognition associations.
resultsαSyn positivity (19.0%) amplified the amyloid-tau association across all Braak stages (meta-temporal interaction β = 0.258, 95% CI 0.104-0.411, p = 0.001), with strongest effects in Braak III-IV. αSyn did not modify tau-cognition associations in any domain (all interaction p > 0.18). DISCUSSION: αSyn co-pathology selectively amplifies amyloid-driven tau propagation without modifying downstream tau-cognition relationships, identifying a node-specific effect within the ATN cascade with implications for patient stratification.
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