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Nicotine therapy: whether a good or bad move in Parkinsonism in concert with HSPs?

Author(s): Pravir Kumar1, 3, *, Shalini Pal1, R. Karunya1 and Rashmi Ambasta2

Journal: Journal of Pharmacy Research
ISSN 0974-6943

Volume: 4;
Issue: 10;
Start page: 3514;
Date: 2011;
Original page

Keywords: Parkinson’s disease | Nicotinic acetylcholine receptors | Heat Shock Proteins | Neuronal nicotinic acetylcholine receptor | Nicotine therapy

Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder, impairs the motor activities in patient. Increasing evidences reveal the nicotineadministration has neuroprotective rather than neurorestorative effect in PD. PD is largely characterized by a decline in nicotinic acetylcholine receptors(nAChRs) and affected nicotinic cholinergic system. Stimulation of nAChRs located on pre-synaptic dopaminergic neurons by nicotine increases dopamine releasein the striatum. Rat and monkey models were used where rats were pre- and post-administered with nicotine and 6-OHDA [31]. Here nicotinic pre treatmentattenuated the behavioral defects and lesion induced loss of striatal dopamine transfer. However, chronic nicotine treatment differentially regulates striatal nAChRsexpression and function [59]. Chronic nicotine treatment via drinking water increased the burst and non- burst endogenous dopamine release in the animal models.Moreover, nicotine administration in mice up regulates levels of Rynodine receptor-2 (RyR-2) thereby affecting an individual’s cognitive and addictive properties[89]. Growing awareness in the field of molecular chaperones can be an additive value to treat the PD in association with nicotine. However, little is known aboutthe effect of nicotine on heat shock proteins (HSPs) under stressed condition. In this review, we focus on the beneficial effects of nicotine as a therapeutic moleculeto minimize the risk of PD. Conversely, exposure of nicotine is a major concern for PD therapy hence, it is necessary to understand the biology behind thethreshold of nicotine intake by a PD patient so that it does not exert any debilitating effect as a potential carcinogen.
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