ICAR Research Data Repository for Knowledge Management

Parkinson´s disease (PD) is a progressive,neurodegenerative disorder that is characterized by the severe motor symptoms, including uncontrollable tremor, postural imbalance,slowness of movement and rigidity. The main pathological hallmark of
PD is a pronounced loss of dopamine-producing neurons in the
substantia nigra (SN), which results in a drastic decrease in dopamine in the striatum, to which these neurons project.
The etiology of PD has not been fully understood. Unproven
hypotheses have included environmental toxins including metals, pesticides etc and genetic factors. It is proposed that a cross-talk of environmental and genetic factors may be playing a role in causing PD. A variety of mechanisms that are believed to cause accelerated cell death have also been suggested, including oxidative stress, excitotoxicity and mitochondrial dysfunction. Pathologically, PD is
characterized by the loss of the pigmented dopaminergic neurons from the substantia nigra pars compacta, the presence of extracellular melanin (a dark pigment), released from degenerating neurons, reactive gliosis (increase in numbers of glial or support cells), and pink-staining cellular inclusions known as Lewy Bodies.The exact causes and molecular pathogenesis of PD is largely
undefined. However, accumulating evidence suggest the involvement of protein conformational deficit (α-synuclein toxicity), metal toxicity,oxidative stress, DNA instability etc. We focused on the DNA topology and stability and α-synuclein-DNA interactions in the present investigation.