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Physiological and pathological functions of TMEM106B: a gene associated with brain aging and multiple brain disorders
Open accessAbstract
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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“Interestingly, both GRN and TMEM106B are reported to be involved in defective endosome/lysosome trafficking/function49,50, a defect that is also observed in AD.”
From New insights into the genetic etiology of Alzheimer’s disease and related dementias (2022) · cites this paper as [50]
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“we examined TMEM106B 101-103 and necroptosis effector MLKL 104,105 (Fig. 5c-d), two molecules previously implicated in neurodegeneration of AD, and detected no significant changes.”
From NAD+ hydrolase Sarm1 is a key driver of synapse degeneration and memory loss in Alzheimer’s disease (2025) · cites this paper as [103]
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The Progression of Prion Diseases Is Not Altered in the Absence of TMEM106B
Bravo‐Risi, F., Orta, G. A., Kim, P. J., Wylie-Young, H., Stimming, T. H., Soto, P., Estrada, L. D., Jankowsky, J. L., & Morales, R. (2026) · eNeuro · doi:10.1523/eneuro.0043-26.2026
Metadata
- Authors
- Feng, T., Lacrampe, A., & Hu, F.
- Affiliations
- Cornell University (US)
- Corresponding author
- Hu, Fenghua
- Venue
- Acta Neuropathologica
- Published
- 2021-01-01
- Volume
- 141
- Issue
- 3
- Pages
- 327-339
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC8049516
- OpenAlex
- W3114567345
- Cited by
- 110
- References
- 94
- Citations by year
- 2026: 13 · 2025: 27 · 2024: 25 · 2023: 25 · 2022: 13 · 2021: 6
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS088448 & R01NS095954)
- the Bluefield project to cure frontotemporal dementia
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Health Sciences › Medicine › Genetics (clinical) › Lysosomal Storage Disorders Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- TMEM106B, lysosomal function, lysosomal pH, lysosomal trafficking, lysosome exocytosis, hypomyelinating leukodystrophy, frontotemporal lobar degeneration, limbic-predominant age-related TDP-43 encephalopathy, brain aging, myelination defects, neurodegenerative diseases
- MeSH terms
- Aging, Animals, Brain, Brain Diseases, Humans, Membrane Proteins, Nerve Tissue Proteins
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