Role of Oxidative Stress in Parkinson's Disease

Pars compacta Neuromelanin
DOI: 10.5607/en.2013.22.1.11 Publication Date: 2013-04-08T11:15:31Z
ABSTRACT
Parkinson's disease (PD) is a progressive neurodegenerative movement disorder associated with selective loss of the dopamine(DA)rgic neurons in substantia nigra pars compacta and degeneration projecting nerve fibers striatum. Because there currently no therapy that delays process, modification course by neuroprotective an important unmet clinical need. Toward this end, understanding cellular mechanisms render nigral particularly vulnerable have been subject intensive research. Increasing evidence suggests oxidative stress plays major role. The metabolism DA itself contributes to stress, resulting intracellular macromolecules whose functions are for cell survival. Mitochondrial dysfunction consequent increase reactive oxygen species also trigger sequence events leads demise. In addition, activated microglia produce nitric oxide superoxide during neuroinflammatory responses, aggravated molecules released damaged DAergic such as α-synuclein, neuromelanin matrix metalloproteinase-3. Ways reduce therefore can provide therapeutic strategy. NAD(P)H:quinone reductase (NQO1) other antioxidant enzymes, gene expression commonly under regulation transcription factor Nrf2, serve target proteins utilized toward development disease-modifying PD.
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