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

Carol E. Peyser, Marshal Folstein, Gary A. Chase, Sergio Starkstein, Jason Brandt, Joseph R. Cockrell, Fred Bylsma, Joseph T. Coyle, Paul R. McHugh, Susan E. Folstein

Research output: Contribution to journalArticlepeer-review

Abstract

Objective: 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 α-tocopherol, which reduces oxyradical damage to cell membranes, might slow the course of Huntington's disease. Method: A prospective, double-blind; placebo-controlled study of high-dose d-α-tocopherol treatment was carried out with a cohort of 73 patients with Huntington's disease who were randomly assigned to either d-α-tocopherol or placebo. Patients were monitored for changes in neurologic and neuropsychologic symptoms. Results: Treatment with d-α-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. Conclusions: Antioxidant therapy may slow the rate of motor decline early in the course of Huntington's disease.

Original languageEnglish (US)
Pages (from-to)1771-1775
Number of pages5
JournalAmerican Journal of Psychiatry
Volume152
Issue number12
DOIs
StatePublished - Dec 1995

ASJC Scopus subject areas

  • Psychiatry and Mental health

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