ICAR Research Data Repository for Knowledge Management

Alzheimer's disease (AD) is a complex neurodegenerative disorder of multiple etiology. It is a devastating dementia, correlated with a region specific
neuronal cell loss. The complex neuropathology includes cortical atrophy,formation of neurofibrillary tangles, deposition of amyloid β peptide (Aβ) in senile plaques, synaptic loss, oxidative stress, metal deposition, and apoptosis and all these coupled events lead to the neuronal loss. Despite progress in uncovering many of the factors that contribute to the etiology of the disease,the cause of the nerve cell death still remains unknown. It is very well
accepted that conformational changes in the proteins namely Aβ play an important role in the neurodegeneration of AD, however little is known about the DNA conformational alteration. The changes in the genetic material of AD,
so far documented are, i) mutations in genes, amyloid precursor protein (APP),presenilin-1 (PS-1) and presenilin-2 (PS-2), ii) shift in the DNA from a potentially transcribable euchromatic state to a condensed and probably
heterochromatic state, iii) oxidative damage as revealed by damaged products namely 8-OH Guanosine and 8-OH Cytosine and iv) genetic imbalance caused by the tetraploidy status of the genome by the way of unusual replication before the cell death . However there is no data on DNA topology in AD brain. Hence the present study aimed to understand studies
pertaining to DNA topology and Aβ-DNA interactions in relevance to neurodegeneration in AD brain.