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William R. Markesbery, MD

Arch Neurol. 1999;56:1449-1452.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Increasing evidence demonstrates that oxidative stress causes damage to cell function with aging and is involved in a number of age-related disorders including atherosclerosis, arthritis, and neurodegenerative disorders. In the neurodegenerative diseases, oxidative stress has been implicated in amyotrophic lateral sclerosis, Parkinson disease, Huntington disease, and Alzheimer disease (AD). The neurodegenerative disorder receiving the most attention has been AD, in which an increase occurs in oxidation of brain lipids, carbohydrates, proteins, and DNA. Some of the products of oxidation have been found in the major histopathologic alterations in AD: the neurofibrillary tangles (NFTs) and senile plaques (reviewed in Markesbery and Carney¹ and Ceballos-Picot²). These oxidative modifications are closely associated with a subtle inflammatory process in the brain in AD.

Oxidative stress refers to a state in which free radicals and their products are in excess of antioxidant defense mechanisms. This imbalance can occur as a . . . [Full Text of this Article]

LIPID PEROXIDATION

PROTEIN OXIDATION

DNA OXIDATION

GLYCO-OXIDATION

ENDOGENOUS ANTIOXIDANTS IN AD

CELL CULTURE AND TRANSGENIC ANIMAL EXPERIMENTS

From the Sanders-Brown Center on Aging, Departments of Pathology and Neurology, University of Kentucky Medical Center, Lexington.

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