Trial of d-alpha-tocopherol in Huntington's disease

• Published in: The American journal of psychiatry Vol. 152; no. 12; p. 1771
• Main Authors: Peyser, C E, Folstein, M, Chase, G A, Starkstein, S, Brandt, J, Cockrell, J R, Bylsma, F, Coyle, J T, McHugh, P R, Folstein, S E
• Format: Journal Article
• Language: English
• Published: United States 01-12-1995
• Subjects: Antioxidants - therapeutic use; Chromosomes, Human, Pair 4 - genetics; Double-Blind Method; Humans; Huntington Disease - drug therapy; Huntington Disease - genetics; Isomerism; Oxidative Stress - drug effects; Placebos; Prospective Studies; Treatment Outcome; Vitamin E - pharmacology; Vitamin E - therapeutic use
• ISSN: 0002-953X
• DOI: 10.1176/ajp.152.12.1771

Evidence suggests that the neuropathology of Huntington's disease, a neuropsychiatric disorder due to a mutation on chromosome 4, results from excessive activation of glutamate-gated ion channels, which kills neurons by oxidative stress. Therefore, the authors hypothesized that alpha-tocopherol, which reduces oxyradical damage to cell membranes, might slow the course of Huntington's disease.
A prospective, double-blind; placebo-controlled study of high-dose d-alpha-tocopherol treatment was carried out with a cohort of 73 patients with Huntington's disease who were randomly assigned to either d-alpha-tocopherol or placebo. Patients were monitored for changes in neurologic and neuropsychologic symptoms.
Treatment with d-alpha-tocopherol had no effect on neurologic and neuropsychiatric symptoms in the treatment group overall. However, post hoc analysis revealed a significant selective therapeutic effect on neurologic symptoms for patients early in the course of the disorder.
Antioxidant therapy may slow the rate of motor decline early in the course of Huntington's disease.