Antioxidant therapy in neurologic disease.
Free radical or oxidative injury may be a fundamental mechanism underlying a number of human neurologic diseases. Therapy using free radical scavengers (antioxidants) has the potential to prevent, delay, or ameliorate many neurologic disorders. However, the biochemistry of oxidative pathobiology is complex, and optimum antioxidant therapeutic options may vary and need to be tailored to individual diseases. In vitro and animal model studies support the potential beneficial role of various antioxidant compounds in neurologic disease. However, the results of clinical trials using various antioxidants, including vitamin E, tirilazad, N-acetylcysteine, and ebselen, have been mixed. Potential reasons for these mixed results include lack of pretrial dose-finding studies and failure to appreciate and characterize the individual unique oxidative processes occurring in different diseases. Moreover, therapy with antioxidants may need to be given early in chronic insidious neurologic disorders to achieve an appreciable clinical benefit. Predisease screening and intervention in at-risk individuals may also need to be considered in the near future.
Delanty
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Department of Clinical Neurological Sciences, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland. normandelanty@eircom.net
Dichter
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D000975:Antioxidants / Q000627:therapeutic use*; D001927:Brain Diseases / Q000188:drug therapy* / Q000378:metabolism*; D016166:Free Radical Scavengers / Q000627:therapeutic use; D020441:Ginkgo biloba / Q000627:therapeutic use; D006801:Humans; D016877:Oxidants / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D008517:Phytotherapy; D010946:Plants, Medicinal; D014810:Vitamin E / Q000627:therapeutic use
D000975:Antioxidants; D016166:Free Radical Scavengers; D016877:Oxidants; D014810:Vitamin E