ReviewActa neuropathologica2016
What we know about TMEM106B in neurodegeneration.
Review in Acta neuropathologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.
- Genetic architecture of epigenetic cortical clock age in brain tissue from older individuals: alterations inEpigenetics · 2024Pooled it
- TMEM106B is a selective modulator of TDP-43 pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Genetic frontotemporal degeneration across the lifespan? A critical appraisal of the neurodevelopmental hypothesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Neurodegeneration risk variants promote lysosomal TMEM106B fibril accumulation.bioRxiv : the preprint server for biology · 2026Article
- Granulin loss and TMEM106B risk converge on lysosomal C-terminal fragment pathology in frontotemporal dementia.bioRxiv : the preprint server for biology · 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
- Gerstmann-Sträussler-Scheinker syndrome with unexpected concomitantFrontiers in neuroscience · 2026Article
- Genetic variation in TMEM106B alters microglial activation and cytokine responses in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- Divergent and convergent TMEM106B pathology in murine models of neurodegeneration and human disease.Acta neuropathologica communications · 2025Article
- Disease-modifying effects of TMEM106B in genetic frontotemporal dementia: a longitudinal GENFI study.Brain : a journal of neurology · 2025Article
- LncRNA-induced lysosomal localization of NHE1 promotes increased lysosomal pH in macrophages leading to atherosclerosis.The Journal of biological chemistry · 2025Article
- Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health.Molecular neurodegeneration · 2025Article
- Risk and progression of frontotemporal dementia in carriers of the TMEM106B protective genotype and its relationship with TDP-43 pathology.Annals of translational medicine · 2024Article
- Two novel variants in GRN: the relevance of CNV analysis and genetic screening in FTLD patients with a negative family history.Journal of neurology · 2024Article
- Cleaved TMEM106B forms amyloid aggregates in central and peripheral nervous systems.Acta neuropathologica communications · 2024Article
- TMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy.bioRxiv : the preprint server for biology · 2024Article
- Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.Journal of neuropathology and experimental neurology · 2024Review
- Physiological and pathological functions of TMEM106B in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Gene specific effects on brain volume and cognition ofmedRxiv : the preprint server for health sciences · 2024Article
- TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy.Acta neuropathologica · 2024Article
18 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Frontotemporal lobar degeneration is a neurodegenerative disorder affecting over 50,000 people in the United States alone. The most common pathological subtype of FTLD is the presence of ubiquitinated TAR DNA binding protein 43 (TDP-43) accumulations in frontal and temporal brain regions at autopsy. While some cases of FTLD-TDP can be attributed to the inheritance of disease-causing mutations, the majority of cases arise with no known genetic cause. In 2010, the first genome-wide association study was conducted in patients with FTLD-TDP to determine potential genetic risk factors for this homogenous subgroup of dementia patients, leading to the identification of the TMEM106B locus on chromosome 7. In this manuscript, we review the initial discovery and replication studies describing TMEM106B variants as disease risk factors and modifiers in TDP-43 proteinopathies, such as FTLD-TDP caused by progranulin (GRN) or chromosome 9 open reading frame 72 (C9orf72) mutations, as well as Alzheimer's disease and hippocampal sclerosis. We further summarize what is currently known about the previously uncharacterized TMEM106B protein and its role as a potential regulator of lysosomal function, and we discuss how modifying TMEM106B levels might uncover promising therapeutic strategies for individuals suffering from TDP-43 proteinopathy.
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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.