ISSN

2277 - 3282

e ISSN

2277 - 3290

Publisher

Journal of Science

OXIDATIVE STRESS, MITOCHONDRIAL DAMAGE & ALZHEIMER’S DISEASE: A COMPLICATED TRIO
Author / Afflication
Vinay Thakur

Govt. College of Pharmacy, Rohru, Distt. Shimla-171207, Himachal Pradesh, India
Vivek Sharma

Govt. College of Pharmacy, Rohru, Distt. Shimla-171207, Himachal Pradesh, India
Rajender Guleria

Govt. College of Pharmacy, Rohru, Distt. Shimla-171207, Himachal Pradesh, India
Keywords
Dementia ,Mitochondria ,Oxidative stress ,
Abstract

Oxidative stress has been implicated in the pathophysiology of many neurological and neurodegenerative diseases. Alzheimer's disease (AD) is the most common neurodegenerative complication and also the most common form of dementia. AD is a chronic, progressive, debilitating neuropsychiatric course of which there is no current effective disease modifying therapy. Acetylcholinesterase inhibitors and N-methyl-D-aspartate glutamate receptor antagonists are the only current standards of therapy. These may mildly improve quality of life but have generally been disappointing and are associated with severe life threatening complications. Inflammation has been at the center stage of AD pathogenesis for a long time but failure of NSAIDs and steroids in several studies has challenged the current hypothesis. Although many questions remain unanswered regarding the pathogenesis of this disease and its relation to aging yet oxidative stress seem to play an important and decisive role. Cells in tissues and organs are continuously subjected to oxidative stress and free radicals on a continuous basis. This free radical attack has exogenous or endogenous (intracellular) origin. The cells withstand and counteract this occurrence by the use of several and different defense mechanisms ranging from free radical scavengers like glutathione, vitamins C and E and antioxidant enzymes like catalase, superoxide dismutase and various peroxidases to sophisticated DNA repair mechanisms. The disturbance in this dynamic equilibrium results in induction of oxidatively induced DNA damage and a variety of lesions of small to high importance. Despite these evidence and clinical approaches in using antioxidant therapy in dementia and AD, researchers have failed to prove a clear benefit for antioxidant treatment in dementia. Hence, there is a need and curiosity as well to understand the disease modifying approach by targeting the oxidant mechanisms in AD

Volume / Issue / Year

4 , 6 , 2014

Starting Page No / Endling Page No

350 - 356