Abstract
BACKGROUND: Alzheimers disease (AD) is a devastative neurodegenerative disorder. Lack of substantial animal model that can unravel molecular underpinnings has been a major lacuna which limited the understanding of the etiology of the disease in turn limiting the employment of potential therapeutic strategies to combat the disease for a few decades. Our studies for the first time provided substantial animal model and tattered the etiology of the disease at a molecular level. METHODS: In this study DNA was isolated from Hippocampus (H), Midbrain (M) and Frontal Cortex (Fc) of control and aluminium maltolate (Al-M) treated aged New Zealand rabbit brain. DNA damage has been studied using Agarose gel electrophoresis, Ethidium Bromide (EtBr) binding and Melting temperature techniques. RESULTS: Al-M treated aged New Zealand rabbit's H and M showed higher DNA damage compared to corresponding controls, where as Fc showed mild DNA damage compared to corresponding controls. CONCLUSIONS: This study tangibly provides substantial molecular level understanding of the disease in turn providing an adequate platform to streamline potential therapeutic strategies. KEYWORDS: Alzheimer's disease; Aluminium maltolate; Animal model; DNA damage.