Associated Papers
Efficient induction of motor neuron disease in transgenic G93A SOD1 mice by prion-like seeding.
Xu G et al.
Prion, 2026
Dysbiosis and Neurodegeneration in ALS: Unraveling the Gut-Brain Axis.
Sharma VK
Neuromolecular Medicine, 2025
Variation in the vulnerability of mice expressing human superoxide dismutase 1 to prion-like seeding: a study of the influence of primary amino acid sequence.
Ayers JI et al.
Acta Neuropathologica Communications, 2021
Are Astrocytes the Predominant Cell Type for Activation of Nrf2 in Aging and Neurodegeneration?
Liddell JR
Antioxidants (basel, Switzerland), 2017
Distinct conformers of transmissible misfolded SOD1 distinguish human SOD1-FALS from other forms of familial and sporadic ALS.
Ayers JI et al.
Acta Neuropathologica, 2016
Prion-like propagation of mutant SOD1 misfolding and motor neuron disease spread along neuroanatomical pathways.
Ayers JI et al.
Acta Neuropathologica, 2016
Biology of mitochondria in neurodegenerative diseases.
Martin LJ
Progress in Molecular Biology and Translational Science, 2012
Dorfin ameliorates phenotypes in a transgenic mouse model of amyotrophic lateral sclerosis.
Sone J et al.
Journal of Neuroscience Research, 2010
Destabilizing protein polymorphisms in the genetic background direct phenotypic expression of mutant SOD1 toxicity.
Gidalevitz T et al.
Plos Genetics, 2009
Loss of metal ions, disulfide reduction and mutations related to familial ALS promote formation of amyloid-like aggregates from superoxide dismutase.
Oztug Durer ZA et al.
Plos One, 2009
How do ALS-associated mutations in superoxide dismutase 1 promote aggregation of the protein?
Shaw BF et al.
Trends in Biochemical Sciences, 2007
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