ReviewActa neuropathologica2022
Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease.
Review in Acta neuropathologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 46 citations in OpenAlex.
- A new era of genome-wide association studies in the field of Alzheimer's disease and overlapping co-pathologies: lessons learned from a neuropathology-centered approach.Acta neuropathologica · 2026Review
- Structural Hierarchy and Maturation of Amyloid Fibrils Revealed by Interface Descriptor Analysis.Journal of chemical information and modeling · 2026Article
- Neurodegeneration risk variants promote lysosomal TMEM106B fibril accumulation.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
- The role of endolysosomal progranulin and TMEM106B in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health.Molecular neurodegeneration · 2025Article
- Progranulin deficiency in the brain: the interplay between neuronal and non-neuronal cells.Translational neurodegeneration · 2025Review
- TMEM106B deficiency leads to alterations in lipid metabolism and obesity in the TDP-43Communications biology · 2025Article
- TMEM106B amyloid filaments in the Biondi bodies of ependymal cells.Acta neuropathologica · 2024Article
- Gene-Specific Effects on Brain Volume and Cognition ofNeurology · 2024Article
- Lysosomal TMEM106B interacts with galactosylceramidase to regulate myelin lipid metabolism.Communications biology · 2024Article
- Cryo-EM structures of pathogenic fibrils and their impact on neurodegenerative disease research.Neuron · 2024Review
- 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
- 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
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 1 institution in 1 country.
Funding
Abstract
Since the initial identification of TMEM106B as a risk factor for frontotemporal lobar degeneration (FTLD), multiple genetic studies have found TMEM106B variants to modulate disease risk in a variety of brain disorders and healthy aging. Neurodegenerative disorders are typically characterized by inclusions of misfolded proteins and since lysosomes are an important site for cellular debris clearance, lysosomal dysfunction has been closely linked to neurodegeneration. Consequently, many causal mutations or genetic risk variants implicated in neurodegenerative diseases encode proteins involved in endosomal-lysosomal function. As an integral lysosomal transmembrane protein, TMEM106B regulates several aspects of lysosomal function and multiple studies have shown that proper TMEM106B protein levels are crucial for maintaining lysosomal health. Yet, the precise function of TMEM106B at the lysosomal membrane is undetermined and it remains unclear how TMEM106B modulates disease risk. Unexpectedly, several independent groups recently showed that the C-terminal domain (AA120-254) of TMEM106B forms amyloid fibrils in the brain of patients with a diverse set of neurodegenerative conditions. The recognition that TMEM106B can form amyloid fibrils and is present across neurodegenerative diseases sheds new light on TMEM106B as a central player in neurodegeneration and brain health, but also raises important new questions. In this review, we summarize current knowledge and place a decade's worth of TMEM106B research into an exciting new perspective.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.