Associated Papers
An ALS-associated mutant SOD1 protein can be eliminated in microglia culture by selective autophagy.
Murakami K et al.
Neuroscience, 2026
Large-scale gene expression changes in APP/PSEN1 and GFAP mutation models exhibit high congruence with Alzheimer's disease.
Gammie SC et al.
Plos One, 2024
5-Hydroxytryptamine: a potential therapeutic target in amyotrophic lateral sclerosis.
Jiang SS et al.
Neural Regeneration Research, 2023
GPX4 deficiency-dependent phospholipid peroxidation drives motor deficits of ALS.
Tu LF et al.
Journal of Advanced Research, 2023
Unique molecular features and cellular responses differentiate two populations of motor cortical layer 5b neurons in a preclinical model of ALS.
Moya MV et al.
Cell Reports, 2022
Are Astrocytes the Predominant Cell Type for Activation of Nrf2 in Aging and Neurodegeneration?
Liddell JR
Antioxidants (basel, Switzerland), 2017
Prion-like propagation of mutant SOD1 misfolding and motor neuron disease spread along neuroanatomical pathways.
Ayers JI et al.
Acta Neuropathologica, 2016
Multiple systemic transplantations of human amniotic mesenchymal stem cells exert therapeutic effects in an ALS mouse model.
Sun H et al.
Cell and Tissue Research, 2014
Expression of wild-type human superoxide dismutase-1 in mice causes amyotrophic lateral sclerosis.
Graffmo KS et al.
Human Molecular Genetics, 2013
Genetic rodent models of amyotrophic lateral sclerosis.
Van Den Bosch L
Journal of Biomedicine & Biotechnology, 2011
Dorfin ameliorates phenotypes in a transgenic mouse model of amyotrophic lateral sclerosis.
Sone J et al.
Journal of Neuroscience Research, 2010
Proteomic characterization of lipid raft proteins in amyotrophic lateral sclerosis mouse spinal cord.
Zhai J et al.
The Febs Journal, 2009
Neuron-specific expression of mutant superoxide dismutase is sufficient to induce amyotrophic lateral sclerosis in transgenic mice.
Jaarsma D et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2008
Motor neuron disease in mice expressing the wild type-like D90A mutant superoxide dismutase-1.
Jonsson PA et al.
Journal of Neuropathology and Experimental Neurology, 2006
Early signs of motoneuron vulnerability in a disease model system: Characterization of transverse slice cultures of spinal cord isolated from embryonic ALS mice.
Avossa D et al.
Neuroscience, 2006
Effect of ubiquitin expression on neuropathogenesis in a mouse model of familial amyotrophic lateral sclerosis.
Gilchrist CA et al.
Neuropathology and Applied Neurobiology, 2005
Mutant SOD1 causes motor neuron disease independent of copper chaperone-mediated copper loading.
Subramaniam JR et al.
Nature Neuroscience, 2002
Disease mechanisms revealed by transcription profiling in SOD1-G93A transgenic mouse spinal cord.
Olsen MK et al.
Annals of Neurology, 2001
Distinct expression and regulation of the glutamate transporter isoforms GLT-1a and GLT-1b in cultured astrocytes from a rat model of amyotrophic lateral sclerosis (hSOD1G93A).
Goursaud S et al.
Neurochemistry International, 0
Superoxide dismutase and neurofilament transgenic models of amyotrophic lateral sclerosis.
Morrison BM et al.
The Journal of Experimental Zoology, 0