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Figure 4 from Mutant superoxide dismutase 1 (SOD1), a cause of amyotrophic  lateral sclerosis, disrupts the recruitment of SMN, the spinal muscular  atrophy protein to nuclear Cajal bodies. | Semantic Scholar
Figure 4 from Mutant superoxide dismutase 1 (SOD1), a cause of amyotrophic lateral sclerosis, disrupts the recruitment of SMN, the spinal muscular atrophy protein to nuclear Cajal bodies. | Semantic Scholar

Murine Models of Neurodegenerative Diseases - Maze Engineers
Murine Models of Neurodegenerative Diseases - Maze Engineers

Molecules | Free Full-Text | A Novel Anti-Inflammatory d-Peptide Inhibits  Disease Phenotype Progression in an ALS Mouse Model
Molecules | Free Full-Text | A Novel Anti-Inflammatory d-Peptide Inhibits Disease Phenotype Progression in an ALS Mouse Model

Tempol improves neuroinflammation and delays motor dysfunction in a mouse  model (SOD1G93A) of ALS | Journal of Neuroinflammation | Full Text
Tempol improves neuroinflammation and delays motor dysfunction in a mouse model (SOD1G93A) of ALS | Journal of Neuroinflammation | Full Text

Rodent Amyotrophic Lateral Sclerosis (ALS) Model - Creative Biolabs
Rodent Amyotrophic Lateral Sclerosis (ALS) Model - Creative Biolabs

Frontiers | Circadian Rhythm Dysfunction Accelerates Disease Progression in  a Mouse Model With Amyotrophic Lateral Sclerosis
Frontiers | Circadian Rhythm Dysfunction Accelerates Disease Progression in a Mouse Model With Amyotrophic Lateral Sclerosis

Realizing the gains and losses in C9ORF72 ALS/FTD | Nature Neuroscience
Realizing the gains and losses in C9ORF72 ALS/FTD | Nature Neuroscience

Laboratory Models of ALS - The ALS Association
Laboratory Models of ALS - The ALS Association

TDP-43 mutant transgenic mice develop features of ALS and frontotemporal  lobar degeneration | PNAS
TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration | PNAS

SOD1-G93A Mouse Model - QPS Neuropharmacology
SOD1-G93A Mouse Model - QPS Neuropharmacology

Humanising mice to enable modelling of neurodegenerative diseases | UCL  Queen Square Institute of Neurology - UCL – University College London
Humanising mice to enable modelling of neurodegenerative diseases | UCL Queen Square Institute of Neurology - UCL – University College London

AAV9-mediated gene delivery of MCT1 to oligodendrocytes does not provide a  therapeutic benefit in a mouse model of ALS: Molecular Therapy - Methods &  Clinical Development
AAV9-mediated gene delivery of MCT1 to oligodendrocytes does not provide a therapeutic benefit in a mouse model of ALS: Molecular Therapy - Methods & Clinical Development

Working with ALS Mice: Guidelines for Preclinical Testing and Colony  Management
Working with ALS Mice: Guidelines for Preclinical Testing and Colony Management

Cortical Circuit Dysfunction as a Potential Driver of Amyotrophic Lateral  Sclerosis
Cortical Circuit Dysfunction as a Potential Driver of Amyotrophic Lateral Sclerosis

Boosting the peripheral immune response in the skeletal muscles improved  motor function in ALS transgenic mice - ScienceDirect
Boosting the peripheral immune response in the skeletal muscles improved motor function in ALS transgenic mice - ScienceDirect

MicroRNA-206 Delays ALS Progression and Promotes Regeneration of  Neuromuscular Synapses in Mice | Science
MicroRNA-206 Delays ALS Progression and Promotes Regeneration of Neuromuscular Synapses in Mice | Science

Amyotrophic lateral sclerosis (ALS):SOD1 mouse helps researchers identify  immune component
Amyotrophic lateral sclerosis (ALS):SOD1 mouse helps researchers identify immune component

Human iPSC-derived neural progenitor cells secreting GDNF provide  protection in rodent models of ALS and retinal degeneration - ScienceDirect
Human iPSC-derived neural progenitor cells secreting GDNF provide protection in rodent models of ALS and retinal degeneration - ScienceDirect

Motor neuron disease, TDP-43 pathology, and memory deficits in mice  expressing ALS–FTD-linked UBQLN2 mutations | PNAS
Motor neuron disease, TDP-43 pathology, and memory deficits in mice expressing ALS–FTD-linked UBQLN2 mutations | PNAS

Zuoshang Xu Lab - University of Massachusetts Chan Medical School
Zuoshang Xu Lab - University of Massachusetts Chan Medical School

Opinion: more mouse models and more translation needed for ALS | Molecular  Neurodegeneration | Full Text
Opinion: more mouse models and more translation needed for ALS | Molecular Neurodegeneration | Full Text

A New AAV10-U7-Mediated Gene Therapy Prolongs Survival and Restores  Function in an ALS Mouse Model - ScienceDirect
A New AAV10-U7-Mediated Gene Therapy Prolongs Survival and Restores Function in an ALS Mouse Model - ScienceDirect

Identification of novel neuroprotective molecule effective in ALS mouse  models | The University of Tokyo
Identification of novel neuroprotective molecule effective in ALS mouse models | The University of Tokyo

TDP-43 transgenic mice develop spastic paralysis and neuronal inclusions  characteristic of ALS and frontotemporal lobar degeneration | PNAS
TDP-43 transgenic mice develop spastic paralysis and neuronal inclusions characteristic of ALS and frontotemporal lobar degeneration | PNAS