4.6 Article

Accumulation of TMEM106B C-terminal fragments in neurodegenerative disease and aging

Related references

Note: Only part of the references are listed.
Article Biochemistry & Molecular Biology

Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases

Andrew Chang et al.

Summary: This study demonstrates the presence of amyloid fibrils composed of TMEM106B in various neurodegenerative diseases, suggesting a potential shared fibrillization pathway.
Article Multidisciplinary Sciences

Age-dependent formation of TMEM106B amyloid filaments in human brains

Manuel Schweighauser et al.

Summary: The study found that TMEM106B protein forms amyloid filaments in the brains of patients with various neurodegenerative diseases. The structures of TMEM106B filaments differ in different brain regions and do not show clear associations with specific diseases. The presence of TMEM106B filaments in the brains of older individuals suggests an age-dependent formation pattern, which is not observed in younger individuals with normal neurology.

NATURE (2022)

Article Multidisciplinary Sciences

Amyloid fibrils in FTLD-TDP are composed of TMEM106B and not TDP-43

Yi Xiao Jiang et al.

Summary: This study found that amyloid fibrils in FTLD-TDP patients are formed by TMEM106B protein rather than TDP-43 protein. In addition, abundant non-fibrillar aggregated TDP-43 protein was observed.

NATURE (2022)

Article Neurosciences

TMEM106B deficiency impairs cerebellar myelination and synaptic integrity with Purkinje cell loss

Tuancheng Feng et al.

Summary: In this study, the role of TMEM106B in the cerebellum was investigated. It was found that TMEM106B is widely expressed in neurons, especially in Purkinje neurons. Aged TMEM106B-deficient mice showed significant loss of Purkinje neurons specifically in the anterior lobe of the cerebellum. Myelination defects and a significant loss of synapses between Purkinje and deep cerebellar nuclei neurons were observed in young mice. These findings suggest that TMEM106B is critical for maintaining neuronal function and synaptic integrity in the cerebellum.

ACTA NEUROPATHOLOGICA COMMUNICATIONS (2022)

Review Clinical Neurology

Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease

Jolien Perneel et al.

Summary: TMEM106B is a gene associated with the risk of neurodegenerative diseases and healthy aging. It is involved in lysosomal function and the formation of amyloid fibrils. Research on TMEM106B provides a new perspective on brain disorders and brain health.

ACTA NEUROPATHOLOGICA (2022)

Article Clinical Neurology

Aged Tmem106b knockout mice display gait deficits in coincidence with Purkinje cell loss and only limited signs of non-motor dysfunction

Stijn Stroobants et al.

Summary: The knockout of the TMEM106B gene in aged mice resulted in behavioral deficits such as motor impairment and gait defects, along with neuronal dysfunction in different brain areas. This study sheds light on the role of TMEM106B in maintaining neuronal homeostasis and survival, particularly in Purkinje cells.

BRAIN PATHOLOGY (2021)

Review Clinical Neurology

Physiological and pathological functions of TMEM106B: a gene associated with brain aging and multiple brain disorders

Tuancheng Feng et al.

Summary: TMEM106B, a lysosome membrane protein, is associated with brain aging, neurodegenerative diseases, and regulates various aspects of lysosomal function. Both deficiency and alterations in TMEM106B levels are linked to lysosomal abnormalities and brain disorders.

ACTA NEUROPATHOLOGICA (2021)

Article Clinical Neurology

A novel temporal-predominant neuro-astroglial tauopathy associated with TMEM106B gene polymorphism in FTLD/ALS-TDP

Jorge J. Llibre-Guerra et al.

Summary: Polymorphisms in TMEM106B gene are associated with worse outcomes in FTLD and ALS. Individuals with A/A genotype have a higher risk of developing a specific neuro-astroglial tauopathy.

BRAIN PATHOLOGY (2021)

Letter Clinical Neurology

Loss of Tmem106b leads to cerebellum Purkinje cell death and motor deficits

Rosa Rademakers et al.

BRAIN PATHOLOGY (2021)

Article Neurosciences

Analysis of genes (TMEM106B, GRN, ABCC9, KCNMB2, and APOE) implicated in risk for LATE-NC and hippocampal sclerosis provides pathogenetic insights: a retrospective genetic association study

Adam J. Dugan et al.

Summary: Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is one of the most common subtypes of TDP-43 proteinopathy, often co-occurring with hippocampal sclerosis (HS) pathology, and showing associations with specific genetic variants. Through analyzing the genetic associations with HS, LATE-NC, and Alzheimer's pathologies, significant gene-based associations were found, offering new insights into the differential effects of risk alleles on LATE-NC and HS.

ACTA NEUROPATHOLOGICA COMMUNICATIONS (2021)

Article Biochemistry & Molecular Biology

Loss ofTMEM106B andPGRNleads to severe lysosomal abnormalities and neurodegeneration in mice

Tuancheng Feng et al.

EMBO REPORTS (2020)

Article Clinical Neurology

TMEM106B Effect on cognition in Parkinson disease and frontotemporal dementia

Thomas F. Tropea et al.

ANNALS OF NEUROLOGY (2019)

Letter Clinical Neurology

The TMEM106B risk allele is associated with lower cortical volumes in a clinically diagnosed frontotemporal dementia cohort

Sophie R. Harding et al.

JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY (2017)

Article Genetics & Heredity

A Dementia-Associated Risk Variant near TMEM106B Alters Chromatin Architecture and Gene Expression

Michael D. Gallagher et al.

AMERICAN JOURNAL OF HUMAN GENETICS (2017)

Review Clinical Neurology

What we know about TMEM106B in neurodegeneration

Alexandra M. Nicholson et al.

ACTA NEUROPATHOLOGICA (2016)

Article Clinical Neurology

Reassessment of Risk Genotypes (GRN, TMEM106B, and ABCC9 Variants) Associated With Hippocampal Sclerosis of Aging Pathology

Peter T. Nelson et al.

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY (2015)

Article Clinical Neurology

TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia

Marka van Blitterswijk et al.

ACTA NEUROPATHOLOGICA (2014)

Article Clinical Neurology

TMEM106B expression is reduced in Alzheimer's disease brains

Jun-ichi Satoh et al.

ALZHEIMERS RESEARCH & THERAPY (2014)

Article Biochemistry & Molecular Biology

TMEM106B p.T185S regulates TMEM106B protein levels: implications for frontotemporal dementia

Alexandra M. Nicholson et al.

JOURNAL OF NEUROCHEMISTRY (2013)

Article Neurosciences

Expression of TMEM106B, the frontotemporal lobar degeneration-associated protein, in normal and diseased human brain

Johanna I. Busch et al.

ACTA NEUROPATHOLOGICA COMMUNICATIONS (2013)

Editorial Material Clinical Neurology

TMEM106B RISK VARIANT IS IMPLICATED IN THE PATHOLOGIC PRESENTATION OF ALZHEIMER DISEASE

Nicola J. Rutherford et al.

NEUROLOGY (2012)

Letter Clinical Neurology

A harmonized classification system for FTLD-TDP pathology

Ian R. A. Mackenzie et al.

ACTA NEUROPATHOLOGICA (2011)

Article Genetics & Heredity

Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP43 inclusions

Vivianna M. Van Deerlin et al.

NATURE GENETICS (2010)

Article Biochemistry & Molecular Biology

Common variation in the miR-659 binding-site of GRN is a major risk factor for TDP43-positive frontotemporal dementia

Rosa Rademakers et al.

HUMAN MOLECULAR GENETICS (2008)