FREE RADICAL OXIDATIVE DAMAGE AND ALZHEMEIRS DISEASE

Free radical oxidative damage and Alzhemeirs disease

Abstract

Alzheimer's Disease is a very complex disease that does not appear to have a single cause, but our research indicates that oxidative stress is probably a primary event in the course of the illness. Oxidative stress is thought to play a major role in the pathogenesis of Alzheimer's disease (AD). Although there is strong post-mortem and experimental evidence of oxidative damage occurring in AD brains, the use of markers in the peripheral circulation to show oxidative stress is less convincing. This report seeks to explore the evidence indicating the potential role of free radicals in the development of Alzheimer's disease.

Table of Contents

CHAPTER15

INTRODUCTION5

Free radicals5

Fentons Reaction By Halliwell6

Sources Of Free Radicals6

Different Radical Speices7

Antioxidant System7

Epidemiology of Alzheimer disease7

Classification of disease8

Subgroup of dementia9

Mechanism10

Sign11

CHAPTER 212

METHODOLOGY12

Research Method12

Structured Literature Review12

Identifying key words and search strings12

Selecting search engines13

Identification of the Sources of Information14

Researcher's analysis of the use of the data collected14

Identification of the number of articles selected15

Justification of the number of articles selected15

CHAPTER 316

RESULTS16

Lipid peroxidation in AD16

Protein oxidation in AD brain20

Specifically oxidized proteins in AD brain21

Antioxidant enzymes24

Methionine oxidation24

CHAPTER 426

DISCUSSION26

Conclusion32

REFRENECES34

Chapter1

Introduction

Alzheimer's disease is defined by the National Institute on Aging as progressive, irretrievable declines in memory, performance of habitual everyday jobs, time and space direction, speech and communication skills, theoretical views, and the aptitude to learn and carry out mathematical computations. Other indications comprise of character changes and damaged judgment. The trademark changes of AD are thick deposits (neuritic plaques) of a protein piece called beta amyloid outside the nerve cells (neurons) in the brain, and warped strands (neurofibrillary tangles) of a protein called tau inside the cells.

There is a loss of these neurons' connections (synapses) with other neurons in areas of the brain that are fundamental to memory and other mental abilities. This route is considered to also cause an inflammatory reaction, which has guided to the research of anti-inflammatory medications as an adjunctive therapy. In supplement to the loss of neurons, there are also lower levels of chemicals (neurotransmitters) in the brain that transmit complex messages back and forth between millions of nerve cells.

The etiopathogenesis of Alzheimer's disease (AD) is still unclear. Recent findings indicate that cellular events involving oxidative stress may be a basic mechanism of neurodegenerative disease. Severe oxidative stress progressively leads to cell dysfunction and ultimately cell death. Oxidative stress is an imbalance between pro-oxidants and/or free radicals on one hand, and anti-oxidizing systems on the other (2-7). Oxidative stress results from generation of oxygen free radicals, hydrogen peroxide, hydroxyl radical, hydroperoxide, dioxygen and nitric oxide, collectively termed as reactive oxygen species (ROS). ROS is hypothesized to be main etiologic factor for progressive and specific neuronal degeneration which is observed in the AD . These ROS are highly reactive toward protein, lipids and DNA molecules causing damage to these macromolecules and possibly leading to dysfunction or death of the cell. 

Free radicals

Free radicals are highly reactive molecules or chemical species capable of independent existence. Generation of highly Reactive Oxygen Species (ROS) is an integral feature of normal cellular function like mitochondrial respiratory chain, phagocytosis, arachidonic acid metabolism, ovulation, and ...