ArticleCommunications biology2025
TMEM106B deficiency leads to alterations in lipid metabolism and obesity in the TDP-43
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Distinct Transcriptional States of TDP-43 Pathology in an Alzheimer's Disease Mouse Model.Neuroscience bulletin · 2026Article
- Shared genetic architecture between obesity and psychiatric disorders reveals comorbid etiology and therapeutic targets.Life medicine · 2026Article
- The amyloidogenic C-terminal region of TMEM106B modulates lipid membrane biophysical properties: Functional and pathological insights.The Journal of biological chemistry · 2026Article
- Potential role of different animal models for the evaluation of bioactive compounds.Annals of medicine and surgery (2012) · 2025Review
- TDP-43 dysregulation impairs cholesterol metabolism linked with myelination defects.Acta neuropathologica · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
The TMEM106B gene, encoding a lysosomal membrane protein, is closely linked with brain aging and neurodegeneration. TMEM106B has been identified as a risk factor for several neurodegenerative diseases characterized by aggregation of the RNA-binding protein TDP-43, including frontotemporal lobar degeneration (FTLD) and limbic-predominant age-related TDP-43 encephalopathy (LATE). To investigate the role of TMEM106B in TDP-43 proteinopathy, we ablated TMEM106B in the TDP-43
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Registered trials
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