Early activation of cellular stress and death pathways caused by cytoplasmic TDP-43 in the rNLS8 mouse model of ALS and FTD
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Immunotherapy targeting the C-terminal domain of TDP-43 decreases neuropathology and confers neuroprotection in mouse models of ALS/FTD - ScienceDirect
Multi-phaseted problems of TDP-43 in selective neuronal vulnerability in ALS
The Molecular Link Between TDP-43, Endogenous Retroviruses and Inflammatory Neurodegeneration in Amyotrophic Lateral Sclerosis: a Potential Target for Triumeq, an Antiretroviral Therapy
Neurology International, Free Full-Text
Early activation of cellular stress and death pathways caused by cytoplasmic TDP-43 in the rNLS8 mouse model of ALS/FTD
ER stress and proteasome inhibition cause redistribution of wildtype
Early activation of cellular stress and death pathways caused by cytoplasmic TDP-43 in the rNLS8 mouse model of ALS and FTD
Transgenic TDP-43-NLS mice have an altered polysome profile in brain
(PDF) Microglial transcriptome analysis in the rNLS8 mouse model of TDP-43 proteinopathy reveals discrete expression profiles associated with neurodegenerative progression and recovery
From basic research to the clinic: innovative therapies for ALS and FTD in the pipeline, Molecular Neurodegeneration
Patient-Specific Cells for Modeling and Decoding Amyotrophic Lateral Sclerosis: Advances and Challenges
Riluzole does not ameliorate disease caused by cytoplasmic TDP‐43 in a mouse model of amyotrophic lateral sclerosis - Wright - 2021 - European Journal of Neuroscience - Wiley Online Library
TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD
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