Associated Papers
Association of TMEM106B Gene rs1990622 Polymorphism with Cognitive Impairment in Adolescents with Depressive Disorder.
Zhang C et al.
The Tohoku Journal of Experimental Medicine, 2026
TMEM106B Supports Viral Entry and Syncytia Formation Mediated by the Spike Proteins From Omicron BA.2.86 and JN.1.
Wang Y et al.
Journal of Medical Virology, 2025
Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health.
Perneel J et al.
Molecular Neurodegeneration, 2025
TMEM106B deficiency leads to alterations in lipid metabolism and obesity in the TDP-43Q331K knock-in mouse model.
Yang C et al.
Communications Biology, 2025
Risk and progression of frontotemporal dementia in carriers of the TMEM106B protective genotype and its relationship with TDP-43 pathology.
Gomes KB
Annals of Translational Medicine, 2024
Identifying pathogenic variants in rare pediatric neurological diseases using exome sequencing.
Komatsu K et al.
Scientific Reports, 2024
Lysosomal TMEM106B interacts with galactosylceramidase to regulate myelin lipid metabolism.
Takahashi H et al.
Communications Biology, 2024
Hypomyelination Leukodystrophy 16 (HLD16)-Associated Mutation p.Asp252Asn of TMEM106B Blunts Cell Morphological Differentiation.
Sawaguchi S et al.
Current Issues in Molecular Biology, 2024
Physiological and pathological functions of TMEM106B in neurodegenerative diseases.
Zhu M et al.
Cellular and Molecular Life Sciences : Cmls, 2024
Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.
Feng T et al.
Acta Neuropathologica, 2024
Yield of exome sequencing in patients with developmental and epileptic encephalopathies and inconclusive targeted gene panel.
Sedlackova L et al.
European Journal of Paediatric Neurology : Ejpn : Official Journal of the European Paediatric Neurology Society, 2024
Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.
Feng T et al.
Biorxiv : the Preprint Server for Biology, 2023
The major TMEM106B dementia risk allele affects TMEM106B protein levels, fibril formation, and myelin lipid homeostasis in the ageing human hippocampus.
Lee JY et al.
Molecular Neurodegeneration, 2023
Lysosomal TMEM106B interacts with galactosylceramidase to regulate myelin lipid metabolism.
Takahashi H et al.
Biorxiv : the Preprint Server for Biology, 2023
Molecular Pathogenic Mechanisms of Hypomyelinating Leukodystrophies (HLDs).
Torii T et al.
Neurology International, 2023
Superresolution live-cell imaging reveals that the localization of TMEM106B to filopodia in oligodendrocytes is compromised by the hypomyelination-related D252N mutation.
Xing S et al.
Science China. Life Sciences, 2023
TMEM106B regulates microglial proliferation and survival in response to demyelination.
Zhang T et al.
Science Advances, 2023
Accumulation of TMEM106B C-terminal fragments in neurodegenerative disease and aging.
Perneel J et al.
Acta Neuropathologica, 2023
Lack of a protective effect of the Tmem106b "protective SNP" in the Grn knockout mouse model for frontotemporal lobar degeneration.
Cabron AS et al.
Acta Neuropathologica Communications, 2023
The major TMEM106B dementia risk allele affects TMEM106B protein levels and myelin lipid homeostasis in the ageing human hippocampus.
Lee JY et al.
Research Square, 2023
Identification of a de novo Mutation in TMEM106B in a Saudi Child Causes Hypomyelination Leukodystrophy.
Alotaibi L et al.
Global Medical Genetics, 2023
Solving inherited white matter disorder etiologies in the neurology clinic: Challenges and lessons learned using next-generation sequencing.
Perrier S et al.
Frontiers in Neurology, 2023
Prospect of genetic disorders in Saudi Arabia.
Alqahtani AS et al.
Frontiers in Genetics, 2023
Severe Epilepsy and Movement Disorder May Be Early Symptoms of TMEM106B-Related Hypomyelinating Leukodystrophy.
Solazzi R et al.
Neurology. Genetics, 2022
TMEM106B deficiency impairs cerebellar myelination and synaptic integrity with Purkinje cell loss.
Feng T et al.
Acta Neuropathologica Communications, 2022
Emerging cellular themes in leukodystrophies.
Nowacki JC et al.
Frontiers in Cell and Developmental Biology, 2022
Genetic analysis of 20 patients with hypomyelinating leukodystrophy by trio-based whole-exome sequencing.
Yan H et al.
Journal of Human Genetics, 2021
Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis.
Root J et al.
Neurobiology of Disease, 2021
Physiological and pathological functions of TMEM106B: a gene associated with brain aging and multiple brain disorders.
Feng T et al.
Acta Neuropathologica, 2021
Hypomyelinating leukodystrophies - unravelling myelin biology.
Wolf NI et al.
Nature Reviews. Neurology, 2021
Loss of Tmem106b exacerbates FTLD pathologies and causes motor deficits in progranulin-deficient mice.
Zhou X et al.
Embo Reports, 2020
A recurrent TMEM106B mutation in hypomyelinating leukodystrophy: A rapid diagnostic assay.
Ikemoto S et al.
Brain & Development, 2020
Genetics of Gene Expression in the Aging Human Brain Reveal TDP-43 Proteinopathy Pathophysiology.
Yang HS et al.
Neuron, 2020
A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination.
Feng T et al.
Brain : a Journal of Neurology, 2020
Loss of TMEM106B leads to myelination deficits: implications for frontotemporal dementia treatment strategies.
Zhou X et al.
Brain : a Journal of Neurology, 2020
The lysosomal function of progranulin, a guardian against neurodegeneration.
Paushter DH et al.
Acta Neuropathologica, 2018
The recurrent mutation in TMEM106B also causes hypomyelinating leukodystrophy in China and is a CpG hotspot.
Yan H et al.
Brain : a Journal of Neurology, 2018
Reply: The recurrent mutation in TMEM106B also causes hypomyelinating leukodystrophy in China and is a CpG hotspot.
Simons C et al.
Brain : a Journal of Neurology, 2018
A recurrent de novo mutation in TMEM106B causes hypomyelinating leukodystrophy.
Simons C et al.
Brain : a Journal of Neurology, 2017