|
|
||||||||
Review Article |
1 From the Research Service and GRECC, VA Medical Center, Minneapolis, and the Department of Psychiatry, University of Minnesota, Minneapolis.
Oxidative stress is a putative factor in the pathogenesis of many human disorders of the central nervous system. Therefore, antioxidants such as vitamin E have become attractive as therapeutic agents in the treatment of several diseases. In addition, vitamin E seems to play a specific role in the nervous system. As a result, vitamin E has been used in pharmacologic doses in the treatment of disorders such as Parkinson disease, Alzheimer disease, and tardive dyskinesia. One investigation showed that the use of 2000 IU all-rac-
-tocopheryl acetate is beneficial in the treatment of Alzheimer disease. Similar doses of vitamin E, however, were not beneficial for delaying the progression of Parkinson disease. In other studies, dosages
400 IU vitamin E/d were found to be beneficial in the treatment of tardive dyskinesia, although this finding was not confirmed in a larger cooperative study conducted by the Veterans Administration. Even though the efficacy of vitamin E in the management of cardiovascular disease has been shown, the potential role of vitamin E in the treatment of cerebrovascular disease remains essentially unknown. The experience from 2 large clinical trials involving the oral intake of 2000 IU vitamin E/d suggests that vitamin E is relatively safe at this dosage for periods <2 y. However, the safety and efficacy of supplemental vitamin E over periods of many years in the prevention of neurologic diseases has not been adequately explored.
Key Words: Aged elderly antioxidants central nervous system megadose therapeutic agent
-tocopherol vitamin E Parkinson disease Alzheimer disease cardiovascular disease tardive dyskinesia
This article has been cited by other articles:
![]() |
S. Vale Current Management of the Cognitive Dysfunction in Parkinson's Disease: How Far Have We Come? Experimental Biology and Medicine, August 1, 2008; 233(8): 941 - 951. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Navarro, C. Gomez, M.-J. Sanchez-Pino, H. Gonzalez, M. J. Bandez, A. D. Boveris, and A. Boveris Vitamin E at high doses improves survival, neurological performance, and brain mitochondrial function in aging male mice Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2005; 289(5): R1392 - R1399. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. P. Mattson, S. L. Chan, and W. Duan Modification of Brain Aging and Neurodegenerative Disorders by Genes, Diet, and Behavior Physiol Rev, July 1, 2002; 82(3): 637 - 672. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. B. Gorelick Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy: An Invited Review Stroke, March 1, 2002; 33(3): 862 - 875. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. J Kayden and T. Wisniewski On the biological activity of vitamin E Am. J. Clinical Nutrition, July 1, 2000; 72(1): 201 - 202. [Full Text] |
||||
![]() |
G. T Vatassery, T. Bauer, and M. Dysken Reply to HJ Kayden and T Wisniewski Am. J. Clinical Nutrition, July 1, 2000; 72(1): 202 - 203. [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |