<?xml version="1.0" encoding="UTF-8"?><Articles><Article><id>97</id><JournalTitle>OXIDATIVE STRESS, MITOCHONDRIAL DAMAGE & ALZHEIMERâ€™S DISEASE: A COMPLICATED TRIO</JournalTitle><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</Abstract><Email>viveksharma_pharma@yahoo.co.in</Email><articletype>Review</articletype><volume>4</volume><issue>6</issue><year>2014</year><keyword>Dementia,Mitochondria,Oxidative stress</keyword><AUTHORS>Vinay Thakur,Vivek Sharma,Rajender Guleria</AUTHORS><afflication>Govt. College of Pharmacy, Rohru, Distt. Shimla-171207, Himachal Pradesh, India,Govt. College of Pharmacy, Rohru, Distt. Shimla-171207, Himachal Pradesh, India,Govt. College of Pharmacy, Rohru, Distt. Shimla-171207, Himachal Pradesh, India</afflication></Article></Articles>