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Both human and rodent central nervous systems express the vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>receptor (<jats:styled-content style=\"fixed-case\">VDR<\/jats:styled-content>) and\/or its enzymatic machinery needed to fully activate the hormone. Clinical research suggests that vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>treatment can improve compromised human muscular ability and increase muscle size, supported by loss of motor function and muscle mass in animals following<jats:styled-content style=\"fixed-case\">VDR<\/jats:styled-content>knockout, as well as increased muscle protein synthesis and<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>production following vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>supplementation. Vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>has also been shown to reduce the expression of biomarkers associated with oxidative stress and inflammation in patients with multiple sclerosis, rheumatoid arthritis, congestive heart failure,<jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>arkinson's disease and<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>lzheimer's disease; diseases that share common pathophysiologies with<jats:styled-content style=\"fixed-case\">ALS<\/jats:styled-content>. Furthermore, vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>treatment greatly attenuates hypoxic brain damage<jats:italic>in vivo<\/jats:italic>and reduces neuronal lethality of glutamate insult<jats:italic>in vitro<\/jats:italic>; a hallmark trait of<jats:styled-content style=\"fixed-case\">ALS<\/jats:styled-content>glutamate excitotoxicity. We have recently shown that high\u2010dose vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content><jats:sub>3<\/jats:sub>supplementation improved, whereas vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content><jats:sub>3<\/jats:sub>restriction worsened, functional capacity in the<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>93<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>mouse model of<jats:styled-content style=\"fixed-case\">ALS<\/jats:styled-content>. In sum, evidence demonstrates that vitamin<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>, unlike the antiglutamatergic agent<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>iluzole, affects multiple aspects of<jats:styled-content style=\"fixed-case\">ALS<\/jats:styled-content>pathophysiology and could provide a greater cumulative effect.<\/jats:p>","DOI":"10.1111\/cns.12204","type":"journal-article","created":{"date-parts":[[2014,1,16]],"date-time":"2014-01-16T06:26:17Z","timestamp":1389853577000},"page":"101-111","source":"Crossref","is-referenced-by-count":52,"title":["Vitamin D as a Potential Therapy in Amyotrophic Lateral Sclerosis"],"prefix":"10.1111","volume":"20","author":[{"given":"Alexandro","family":"Gianforcaro","sequence":"first","affiliation":[{"name":"School of Kinesiology and Health Science Faculty of Health, and Muscle Health Research Centre York University Toronto ON 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