ReviewActa neuropathologica2021
Physiological and pathological functions of TMEM106B: a gene associated with brain aging and multiple brain disorders.
Review in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Genetic architecture of epigenetic cortical clock age in brain tissue from older individuals: alterations inEpigenetics · 2024Pooled it
- Article
- Associations between TMEM106B C-terminal fragment aggregation, age, and TDP-43 or tau pathology.Brain pathology (Zurich, Switzerland) · 2026Article
- Chronic traumatic encephalopathy: A devastating legacy of repetitive concussion.Neurobiology of disease · 2026Review
- Shared genetic architecture between obesity and psychiatric disorders reveals comorbid etiology and therapeutic targets.Life medicine · 2026Article
- Colocalization and discordance between plasma and brain protein quantitative trait loci.bioRxiv : the preprint server for biology · 2026Article
- The amyloidogenic C-terminal region of TMEM106B modulates lipid membrane biophysical properties: Functional and pathological insights.The Journal of biological chemistry · 2026Article
- Genetic correlation analysis identifies TMEM106B, ACE, and ERC2 as genetic loci shared between Alzheimer's disease and primary psychiatric disorders.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Review
- LAPTM proteins in neurological disorders - Autophagy-lysosome dysfunction and therapeutic targets: A review.Biomolecules & biomedicine · 2026Review
- A potential drug target in epilepsy and its role in other neurological disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026Review
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Gerstmann-Sträussler-Scheinker syndrome with unexpected concomitantFrontiers in neuroscience · 2026Article
- Mendelian randomization study of the causal relationship between autoimmune diseases and anemia using proteomic and genetic data.Journal of translational autoimmunity · 2025Article
- Genetic variation in TMEM106B alters microglial activation and cytokine responses in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- Convergent Evolution and Host-Limiting Impacts of SARS-CoV-2 Revealed by Cellular Experiments.Molecular biology and evolution · 2025Article
- Molecular mechanisms of SARS-CoV-2 entry: implications for biomedical strategies.Microbiology and molecular biology reviews : MMBR · 2025Review
- Article
- Divergent and convergent TMEM106B pathology in murine models of neurodegeneration and human disease.Acta neuropathologica communications · 2025Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
TMEM106B, encoding a lysosome membrane protein, has been recently associated with brain aging, hypomyelinating leukodystrophy and multiple neurodegenerative diseases, such as frontotemporal lobar degeneration (FTLD) and limbic-predominant age-related TDP-43 encephalopathy (LATE). During the past decade, considerable progress has been made towards our understanding of the cellular and physiological functions of TMEM106B. TMEM106B regulates many aspects of lysosomal function, including lysosomal pH, lysosome movement, and lysosome exocytosis. Both an increase and decrease in TMEM106B levels result in lysosomal abnormalities. In mouse models, TMEM106B deficiency leads to lysosome trafficking and myelination defects and FTLD related pathology. In humans, alterations in TMEM106B levels or function are intimately linked to neuronal proportions, brain aging, and brain disorders. Further elucidation of the physiological function of TMEM106B and changes in TMEM106B under pathological conditions will facilitate therapeutic development to treat brain disorders associated with TMEM106B.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.