Vitamin D as a Potential Therapy in Amyotrophic Lateral Sclerosis

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Summary: VitaminDhas been demonstrated to influence multiple aspects of amyotrophic lateral sclerosis (ALS) pathology. Both human and rodent central nervous systems express the vitaminDreceptor (VDR) and/or its enzymatic machinery needed to fully activate the hormone. Clinical research suggests that vitaminDtreatment can improve compromised human muscular ability and increase muscle size, supported by loss of motor function and muscle mass in animals followingVDRknockout, as well as increased muscle protein synthesis andATPproduction following vitaminDsupplementation. VitaminDhas 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,Parkinson's disease andAlzheimer's disease; diseases that share common pathophysiologies withALS. Furthermore, vitaminDtreatment greatly attenuates hypoxic brain damagein vivoand reduces neuronal lethality of glutamate insultin vitro; a hallmark trait ofALSglutamate excitotoxicity. We have recently shown that high‐dose vitaminD3supplementation improved, whereas vitaminD3restriction worsened, functional capacity in theG93Amouse model ofALS. In sum, evidence demonstrates that vitaminD, unlike the antiglutamatergic agentRiluzole, affects multiple aspects ofALSpathophysiology and could provide a greater cumulative effect.

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