ArticleScience advances2023
TMEM106B regulates microglial proliferation and survival in response to demyelination.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Genetic architecture of epigenetic cortical clock age in brain tissue from older individuals: alterations inEpigenetics · 2024Pooled it
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
- Trem2 activation by renal tubular debris sustains Arg1Frontiers in immunology · 2026Article
- The role of endolysosomal progranulin and TMEM106B in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- LncRNA-induced lysosomal localization of NHE1 promotes increased lysosomal pH in macrophages leading to atherosclerosis.The Journal of biological chemistry · 2025Article
- The effect of Alzheimer's disease genetic factors on limbic white matter microstructure.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- TMEM106B Knockdown Exhibits a Neuroprotective Effect in Parkinson's Disease via Decreasing Inflammation and Iron Deposition.Molecular neurobiology · 2025Article
- Investigating shared risk variants and genetic etiology between Alzheimer's disease and three stress-related psychiatric disorders: a large-scale genome-wide cross-trait analysis.Frontiers in aging · 2025Article
- Association of TMEM106B with CorticalGenes · 2024Article
- Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.Acta neuropathologica · 2024Article
- Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.bioRxiv : the preprint server for biology · 2023Article
- TMEM106B aggregation in neurodegenerative diseases: linking genetics to function.Molecular neurodegeneration · 2023Review
- Lysosomal acidification dysfunction in microglia: an emerging pathogenic mechanism of neuroinflammation and neurodegeneration.Journal of neuroinflammation · 2023Review
- AAV-iScience · 2023Article
- The TMEM106B T186S coding variant increases neurite arborization and synaptic density in primary hippocampal neurons.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
TMEM106B, a lysosomal transmembrane protein, has been closely associated with brain health. Recently, an intriguing link between TMEM106B and brain inflammation has been discovered, but how TMEM106B regulates inflammation is unknown. Here, we report that TMEM106B deficiency in mice leads to reduced microglia proliferation and activation and increased microglial apoptosis in response to demyelination. We also found an increase in lysosomal pH and a decrease in lysosomal enzyme activities in TMEM106B-deficient microglia. Furthermore, TMEM106B loss results in a significant decrease in the protein levels of TREM2, an innate immune receptor essential for microglia survival and activation. Specific ablation of TMEM106B in microglia results in similar microglial phenotypes and myelination defects in mice, supporting the idea that microglial TMEM106B is critical for proper microglial activities and myelination. Moreover, the
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Registered trials
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