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- W2477182457 abstract "Amyotrophic Lateral Sclerosis (ALS) is a fatal motor neuron disease with no cure. Patients experience degeneration of both upper and lower motor neurons, which leads to paralysis and eventual death, usually within 2-5 years of onset. Although ALS was first described in 1824, there remains a lack of a detailed understanding of the mechanisms that culminate in the progressive spread of ALS pathology and subsequent motor neuron loss. Current understanding highlights Cu/Zn superoxide dismutase (SOD1) and transitive response DNA binding protein 43kDa (TDP-43) proteopathies as two of the main pathologies observed in ALS. However, despite the similarities between the two, they have historically been studied in isolation. Here we consider the emerging body of evidence that suggests that the disease mechanisms of the two proteopathies may be linked. We discuss the possibility that insights might be gained from studying the interactions between the two pathologies, instead of continuing to examine them in isolation in order to truly understand ALS pathology." @default.
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- W2477182457 date "2016-05-09" @default.
- W2477182457 modified "2023-09-28" @default.
- W2477182457 title "SOD1 Pathology in ALS: TDP or not TDP that is the Question" @default.
- W2477182457 doi "https://doi.org/10.15406/icpjl.2016.2.00038" @default.
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