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Intrinsic membrane hyperexcitability of amyotrophic lateral sclerosis patient-derived motor neurons. This view is supported to some degree by the observation that the WldS gene, which protects against axonal injury, modestly prolongs survival in the mSOD mouse Fischer et al. These mutations are thought to induce a toxic gain-of-function of the protein, which becomes prone to misfolding and subsequent aggregation. Subsequently, more proximal portions of the axon become affected. Identification of alpha-cardiac myosin heavy chain mRNA and protein in extraocular muscle of the adult rabbit. The relatively early onset of fasciculation in ALS has led to the view that it results from MN excitability and is a marker or consequence of the MN dysfunction Denny-Brown and Pennybacker, ; de Carvalho and Swash, b. These originate, in part, from CST neurons in cortical layer V, whose axons descend to the spinal cord.
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Spencer R, Porter J. Excitatory amino acid neurotoxicity and neurodegenerative disease. Unravelling the enigma of selective vulnerability in neurodegeneration: Motoneurone afterhyperpolarisation time-course following stroke. Type IIb and IIx muscle fibres use glycolysis as their main energy source and display fast-twitch and fast-fatigable properties. This could be explained by the increased susceptibility of the fast motor units to degeneration in ALS Piotrkiewicz and Hausmanowa-Petrusewicz, ; Piotrkiewicz et al. Extraocular muscle itself is more complex, containing many different fibre types, not only those containing the classical skeletal myosins.
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