The finding that AD risk genes (CD33, CR1, PSEN2) are shared risk factors across synucleinopathies challenges the protein-specific disease model, but the mechanistic basis for this cross-disease genetic overlap remains unexplained. This could fundamentally change how we classify neurodegenerative diseases. Gap type: contradiction Source paper: Deep sequencing of proteotoxicity modifier genes uncovers a Presenilin-2/beta-amyloid-actin genetic risk module shared among alpha-synucleinopathies. (2026, bioRxiv : the preprint server for biology, PMID:38496508)
Landscape Summary: Why do Alzheimer's disease genes confer risk across α-synucleinopathies despite different protein aggregates? is a 0.83 priority gap in neurodegeneration. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
Why do Alzheimer's disease genes confer risk across α-synucleinopathies despite different protein aggregates? — INVOKE-2 (completed)
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