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Spinocerebellar ataxias (SCAs) represent a genetically heterogeneous subset of autosomal dominant progressive neurological disorders predominantly caused by expansion of a glutamine-encoding CAG trinucleotide repeat, leading to the accumulation of misfolded proteins, dysfunction of ion channels and mitochondria, and ultimately neurodegeneration, with PCs, brainstem, and spinal cord neurons being particularly affected in SCA type 1 (Watase et al., 2002

Moreover, rodent models are often exposed to UV light at much higher doses than diurnal animals experience environmentally in order to shorten the experimental time course required for the development of cataract

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Moreover, emerging evidence has shown that it participates in many other pathological and physiological processes, including fibrogenesis, ischemic injury, oxidative insult, and aging, as well as in cells in demand for high energy, such as kidney and corneal endothelium

(c) the National Institute on Deafness and Other Communication Disorders (NIDCD) at NIH, under award number T32DC005360 (ZF)