Accumulation of dysfunctional SOD1 protein in Parkinson’s disease is not associated with mutations in the SOD1 gene
Author:
Funder
Parkinson's NSW
Publisher
Springer Science and Business Media LLC
Subject
Cellular and Molecular Neuroscience,Clinical Neurology,Pathology and Forensic Medicine
Link
http://link.springer.com/article/10.1007/s00401-017-1779-6/fulltext.html
Reference11 articles.
1. Bandmann O, Davis MB, Marsden CD, Harding AE (1995) Sequence of the superoxide-dismutase 1 (SOD1) gene in familial Parkinson’s disease. J Neurol Neurosurg Psychiatry 59:90–91. doi: 10.1136/jnnp.59.1.90
2. Da Cruz S, Bui A, Saberi S, Lee SK, Stauffer J, McAlonis-Downes M, Schulte D, Schulte D, Pizzo DP, Parone PA, Cleveland DW et al (2017) Misfolded SOD1 is not a primary component of sporadic ALS. Acta Neuropathol. doi: 10.1007/s00401-017-1688-8 (E-published ahead of print)
3. Davies KM, Bohic S, Carmona A, Ortega R, Cottam V, Hare DJ, Finberg JPM, Reyes S, Halliday GM, Mercer JFB et al (2014) Copper pathology in vulnerable brain regions in Parkinson’s disease. Neurobiol Aging 35:858–866. doi: 10.1016/j.neurobiolaging.2013.09.034
4. Guareschi S, Cova E, Cereda C, Ceroni M, Donetti E, Bosco DA, Trotti D, Pasinelli P (2012) An over-oxidized form of superoxide dismutase found in sporadic amyotrophic lateral sclerosis with bulbar onset shares a toxic mechanism with mutant SOD1. Proc Natl Acad Sci USA 109:5074–5079. doi: 10.1073/pnas.1115402109
5. Hilton JB, White AR, Crouch PJ (2015) Metal-deficient SOD1 in amyotrophic lateral sclerosis. J Mol Med 93:481–487. doi: 10.1007/s00109-015-1273-3
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