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Oxidative stress hypothesis in Alzheimer's disease: a reappraisal.
Trends Pharmacol Sci. 2008 Dec; 29(12):609-15.TP

Abstract

Alzheimer's disease (AD) is the most common form of neurodegenerative disorder with dementia. In its sporadic form, AD results from the combination of genetic factors with different epigenetic events. Among them, oxidative metabolic reactions and their by-products have been consistently implicated in AD pathogenesis and represent the biological basis for the 'oxidative stress hypothesis' of AD. Numerous studies demonstrate that different biomarkers of oxidative-stress-mediated events are elevated in the AD brain. Studies in animal models of the disease with antioxidants report significant improvements of their AD-like phenotype. Although epidemiologic studies show that dietary intake of antioxidants reduces the risk of AD, clinical trials with antioxidants show only a marginal positive or no effect. These conflicting results have created a wave of criticism towards the oxidative stress hypothesis of AD. Here, I review the available data and discuss the necessary paths for a fair reappraisal of the hypothesis.

Authors+Show Affiliations

Department of Pharmacology, Temple University, School of Medicine, Philadelphia, PA 19140, USA. praticod@temple.edu

Pub Type(s)

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

Language

eng

PubMed ID

18838179

Citation

Praticò, Domenico. "Oxidative Stress Hypothesis in Alzheimer's Disease: a Reappraisal." Trends in Pharmacological Sciences, vol. 29, no. 12, 2008, pp. 609-15.
Praticò D. Oxidative stress hypothesis in Alzheimer's disease: a reappraisal. Trends Pharmacol Sci. 2008;29(12):609-15.
Praticò, D. (2008). Oxidative stress hypothesis in Alzheimer's disease: a reappraisal. Trends in Pharmacological Sciences, 29(12), 609-15. https://doi.org/10.1016/j.tips.2008.09.001
Praticò D. Oxidative Stress Hypothesis in Alzheimer's Disease: a Reappraisal. Trends Pharmacol Sci. 2008;29(12):609-15. PubMed PMID: 18838179.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress hypothesis in Alzheimer's disease: a reappraisal. A1 - Praticò,Domenico, Y1 - 2008/10/04/ PY - 2008/07/08/received PY - 2008/08/15/revised PY - 2008/09/09/accepted PY - 2008/10/8/pubmed PY - 2009/6/24/medline PY - 2008/10/8/entrez SP - 609 EP - 15 JF - Trends in pharmacological sciences JO - Trends Pharmacol Sci VL - 29 IS - 12 N2 - Alzheimer's disease (AD) is the most common form of neurodegenerative disorder with dementia. In its sporadic form, AD results from the combination of genetic factors with different epigenetic events. Among them, oxidative metabolic reactions and their by-products have been consistently implicated in AD pathogenesis and represent the biological basis for the 'oxidative stress hypothesis' of AD. Numerous studies demonstrate that different biomarkers of oxidative-stress-mediated events are elevated in the AD brain. Studies in animal models of the disease with antioxidants report significant improvements of their AD-like phenotype. Although epidemiologic studies show that dietary intake of antioxidants reduces the risk of AD, clinical trials with antioxidants show only a marginal positive or no effect. These conflicting results have created a wave of criticism towards the oxidative stress hypothesis of AD. Here, I review the available data and discuss the necessary paths for a fair reappraisal of the hypothesis. SN - 0165-6147 UR - https://www.unboundmedicine.com/medline/citation/18838179/Oxidative_stress_hypothesis_in_Alzheimer's_disease:_a_reappraisal_ DB - PRIME DP - Unbound Medicine ER -