ArticleActa neuropathologica communications2025
Divergent and convergent TMEM106B pathology in murine models of neurodegeneration and human disease.
Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Associations between TMEM106B C-terminal fragment aggregation, age, and TDP-43 or tau pathology.Brain pathology (Zurich, Switzerland) · 2026Article
- TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026Review
- TMEM106B C-terminal fragments drive nucleocytoplasmic transport failure and TDP-43 mislocalization in the aging human brain.bioRxiv : the preprint server for biology · 2026Article
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Abstract
TMEM106B is a lysosome/late endosome protein that is a potent genetic modifier of multiple neurodegenerative diseases as well as general aging. Recently, TMEM106B was shown to form insoluble aggregates in postmortem human brain tissue, drawing attention to TMEM106B pathology and the potential role of TMEM106B aggregation in disease. In the context of neurodegenerative diseases, TMEM106B has been studied in vivo using animal models of neurodegeneration, but these studies rely on overexpression or knockdown approaches. To date, endogenous TMEM106B pathology and its relationship to known canonical pathology in animal models has not been reported. Here, we analyze histological patterns of the endogenous TMEM106B protein in murine models of C9ORF72-related amyotrophic lateral sclerosis and frontotemporal dementia (C9-ALS/FTD), SOD1-related ALS, and tauopathy using an extensively validated TMEM106B antibody. We found profound correlations between the endogenous TMEM106B protein with known TDP-43 and tau pathology in murine models of C9-ALS/FTD and tauopathy, respectively. By using an antibody previously shown to recognize the pathologic TMEM106B C-terminal fragments, we then performed a similar analysis on postmortem brain tissues from patients with C9-ALS/FTD, Alzheimer's disease (AD), and AD with limbic-predominant age-related TDP-43 encephalopathy (AD/LATE). Convergent evidence from both murine models and human patients links TMEM106B to TDP-43 nuclear clearance at the cellular level in C9-ALS. By characterizing endogenous TMEM106B in mice and human postmortem tissue, our work reveals essential considerations that must be taken when analyzing data from in vivo mouse studies and elucidates new insights supporting the involvement of TMEM106B in the pathogenesis and progression of multiple neurodegenerative diseases.
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