Search

Alzheimer's disease is a neurodegenerative disorder with unclear etiology for a few decades. Many animal models employed to study the etiology of the disease and test the efficacy of a drug could give limited understanding of these events. Introduction of aluminum salts into aged New Zealand rabbit brain could demonstrate neurofibrillary tangle formation in 1965. This outstanding contribution substantiated the role of aluminum in Alzheimer's disease in turn becoming the basis further molecular studies in rabbits. In this review, various animal models (transgenic mice, rats, rabbits, zebrafish) used to study the pathology of the disease and to test the efficacy of a drug have been summarized. It also focuses on the growing need to unravel the molecular underpinnings of the disease progression.

Deoxyribonucleic acid (DNA) damage has been implicated in ageing and neurodegenerative disorders including Alzheimer's disease (AD) for a few decades. Although it is an established finding, yet there are limited studies on DNA damage. In both nucleus and mitochondria, DNA damage is primarily free radical mediated. It has been proven that mitochondrial DNA is more vulnerable to damage compared to the nuclear DNA. A few studies summarized in this review throw light on the mechanisms of free radical mediated DNA damage and impairment of DNA repair mechanisms in AD. There is a growing need to initiate studies on DNA damage and repair and unravel the molecular underpinnings entailed in the etiopathogenesis of the disease. The outcome of such studies substantiates the corner stone streamlined to employ therapeutic strategies.