Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health

Characterization of the first transgenic mouse model that overexpresses TMEM106B suggests that higher levels of TMEM106B negatively impacts brain health by modifying brain aging and impairing the resilience of the brain to the pathomechanisms of neurodegenerative disorders. This novel model will be a valuable tool to study the involvement and contribution of increased TMEM106B levels to aging and will be essential to study the many age-related diseases in which TMEM106B was genetically shown to be a disease- and risk-modifier.

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Publication Details

Journal
Molecular Neurodegeneration
Published
2025-04-23
DOI
https://doi.org/10.1186/s13024-025-00831-2
Citations
4
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
3.37

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article

Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health

Debby Van Dam, Ralph B. Perkerson, Linus De Witte, Bavo Heeman et al.
4 citations
Molecular Neurodegeneration
Neuroinflammation and Neurodegeneration Mechanisms
3.37
article

Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health

Debby Van Dam, Ralph B. Perkerson, Linus De Witte, Bavo Heeman, Nemo Peeters, Simona Manzella, Xiaolai Zhou, Rosa Rademakers, Riet De Rycke, Ian R. Mackenzie, Bob Asselbergh, Wouter De Coster, Tommas J. Ellender, Elke Calus, Jolien Perneel, Manuela Neumann, Miranda Lastra Osua, Mieu Brooks, Sara Alidadiani
article en
4 citations

Abstract

Characterization of the first transgenic mouse model that overexpresses TMEM106B suggests that higher levels of TMEM106B negatively impacts brain health by modifying brain aging and impairing the resilience of the brain to the pathomechanisms of neurodegenerative disorders. This novel model will be a valuable tool to study the involvement and contribution of increased TMEM106B levels to aging and will be essential to study the many age-related diseases in which TMEM106B was genetically shown to be a disease- and risk-modifier.

Molecular NeurodegenerationVol. 20(1)
University Medical Center Groningen (NL), Vancouver Coastal Health (CA), University of British Columbia (CA), University of Antwerp (BE), Sun Yat-sen University (CN), University of Groningen (NL), German Center for Neurodegenerative Diseases (DE), Jacksonville College (US), Ghent University (BE), VIB-UAntwerp Center for Molecular Neurology (BE), VIB-UGent Center for Inflammation Research (BE), Mayo Clinic in Florida (US), University of Tübingen (DE)
Mayo Clinic, Neurosearch Antwerp, National Natural Science Foundation of China, Fonds Wetenschappelijk Onderzoek, Natural Science Foundation of Guangdong Province, Vlaams Instituut voor Biotechnologie, Universiteit Antwerpen, Vlaamse regering, National Institutes of Health
Good health and well-being
Openalex Percentile: Top 8%
Neuroinflammation and Neurodegeneration Mechanisms
3.37
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