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Antioxidant strategies for Alzheimer's disease.
Proc Nutr Soc. 2002 May; 61(2):191-202.PN

Abstract

Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from beta-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline observed in AD. Although not a uniformly consistent observation, a number of epidemiological studies have found a link between antioxidant intake and a reduced incidence of dementia, AD and cognitive decline in elderly populations. In AD clinical trials molecules with antioxidant properties such as vitamin E and Ginkgo biloba extract have shown modest benefit. A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment. Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone). Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, beta-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry. Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed.

Authors+Show Affiliations

Grundman M
Alzheimer's Disease Cooperative Study, University of California, San Diego, 8950 Villa La Jolla Drive, Suite 2200, La Jolla, California 92037, USA. mgrundman@ucsd.edu
Grundman M
No affiliation info available
Delaney P
No affiliation info available

MeSH

Alzheimer DiseaseAntioxidantsDietary SupplementsDisease ProgressionDrug Therapy, CombinationGinkgo bilobaHumansOxidation-ReductionOxidative StressVitamin E

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

12133201

Citation

Grundman, Michael, et al. "Antioxidant Strategies for Alzheimer's Disease." The Proceedings of the Nutrition Society, vol. 61, no. 2, 2002, pp. 191-202.
Grundman M, Grundman M, Delaney P. Antioxidant strategies for Alzheimer's disease. Proc Nutr Soc. 2002;61(2):191-202.
Grundman, M., Grundman, M., & Delaney, P. (2002). Antioxidant strategies for Alzheimer's disease. The Proceedings of the Nutrition Society, 61(2), 191-202.
Grundman M, Grundman M, Delaney P. Antioxidant Strategies for Alzheimer's Disease. Proc Nutr Soc. 2002;61(2):191-202. PubMed PMID: 12133201.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Antioxidant strategies for Alzheimer's disease. AU - Grundman,Michael, AU - Grundman,Michael, AU - Delaney,Patrick, PY - 2002/7/23/pubmed PY - 2002/11/26/medline PY - 2002/7/23/entrez SP - 191 EP - 202 JF - The Proceedings of the Nutrition Society JO - Proc Nutr Soc VL - 61 IS - 2 N2 - Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from beta-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline observed in AD. Although not a uniformly consistent observation, a number of epidemiological studies have found a link between antioxidant intake and a reduced incidence of dementia, AD and cognitive decline in elderly populations. In AD clinical trials molecules with antioxidant properties such as vitamin E and Ginkgo biloba extract have shown modest benefit. A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment. Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone). Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, beta-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry. Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed. SN - 0029-6651 UR - https://www.unboundmedicine.com/medline/citation/12133201/Antioxidant_strategies_for_Alzheimer's_disease_ DB - PRIME DP - Unbound Medicine ER -