Description
The abstract shows TMEM106B forms identical fibrils in TDP-43, tau, and α-synuclein diseases, but doesn’t explain why a lysosomal protein aggregates consistently across distinct proteinopathies. Understanding this shared pathway could reveal common therapeutic targets.
Gap type: unexplained_observation Source paper: Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases. (2022, Cell, PMID:35247328)
Evidence summary
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