Associated Papers
TDP-43 dysregulation impairs cholesterol metabolism linked with myelination defects.
García-Toledo I et al.
Acta Neuropathologica, 2025
Challenges of modelling TDP-43 pathology in mice.
Armas JMB et al.
Mammalian Genome : Official Journal of the International Mammalian Genome Society, 2025
Amyotrophic lateral sclerosis caused by TARDBP mutations: from genetics to TDP-43 proteinopathy.
Balendra R et al.
The Lancet. Neurology, 2025
Corrigendum to "TDP-43-M323K causes abnormal brain development and progressive cognitive and motor deficits associated with mislocalised and increased levels of TDP-43" [Neurobiology of disease Volume 193, April 2024, 106437].
Godoy-Corchuelo JM et al.
Neurobiology of Disease, 2024
Elevated nuclear TDP-43 induces constitutive exon skipping.
Carmen-Orozco RP et al.
Molecular Neurodegeneration, 2024
TDP-43-M323K causes abnormal brain development and progressive cognitive and motor deficits associated with mislocalised and increased levels of TDP-43.
Godoy-Corchuelo JM et al.
Neurobiology of Disease, 2024
TDP-43 Epigenetic Facets and Their Neurodegenerative Implications.
Gimenez J et al.
International Journal of Molecular Sciences, 2023
Opinion: more mouse models and more translation needed for ALS.
Fisher EMC et al.
Molecular Neurodegeneration, 2023
Metamorphism in TDP-43 prion-like domain determines chaperone recognition.
Carrasco J et al.
Nature Communications, 2023
Neuronal models of TDP-43 proteinopathy display reduced axonal translation, increased oxidative stress, and defective exocytosis.
Pisciottani A et al.
Frontiers in Cellular Neuroscience, 2023
Molecular Dissection of TDP-43 as a Leading Cause of ALS/FTLD.
Tamaki Y et al.
International Journal of Molecular Sciences, 2022
Nearly 30 Years of Animal Models to Study Amyotrophic Lateral Sclerosis: A Historical Overview and Future Perspectives.
Bonifacino T et al.
International Journal of Molecular Sciences, 2021
Molecular Mechanisms Underlying TDP-43 Pathology in Cellular and Animal Models of ALS and FTLD.
Wood A et al.
International Journal of Molecular Sciences, 2021
Female sex mitigates motor and behavioural phenotypes in TDP-43Q331K knock-in mice.
Watkins J et al.
Scientific Reports, 2020
Focus on the heterogeneity of amyotrophic lateral sclerosis.
Bendotti C et al.
Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration, 2020
FUS ALS-causative mutations impair FUS autoregulation and splicing factor networks through intron retention.
Humphrey J et al.
Nucleic Acids Research, 2020
ALS-linked TDP-43M337V knock-in mice exhibit splicing deregulation without neurodegeneration.
Watanabe S et al.
Molecular Brain, 2020
Dysregulation of TDP-43 intracellular localization and early onset ALS are associated with a TARDBP S375G variant.
Newell K et al.
Brain Pathology (zurich, Switzerland), 2019
Transgenic and physiological mouse models give insights into different aspects of amyotrophic lateral sclerosis.
De Giorgio F et al.
Disease Models & Mechanisms, 2019
TDP-43 mutations increase HNRNP A1-7B through gain of splicing function.
Sivakumar P et al.
Brain : a Journal of Neurology, 2018
Mice with endogenous TDP-43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis.
Fratta P et al.
The Embo Journal, 2018