Nicotine and Parkinson's disease: implications for therapy

Quik, Maryka; O'Leary, Kathryn; Tanner, Caroline M.

doi:10.1002/mds.21900

Cited by 154Parkinson's Disease Mechanisms and TreatmentsNicotinic Acetylcholine Receptors StudyNuclear Receptors and Signaling

Nicotine and Parkinson's disease: implications for therapy

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Quik, Maryka, O'Leary, Kathryn, Tanner, Caroline M.·2008·Movement Disorders

DOI 10.1002/mds.21900PMC PMC4430096

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Abstract

Accumulating evidence suggests that nicotine, a drug that stimulates nicotinic acetylcholine receptors, may be of therapeutic value in Parkinson's disease. Beneficial effects may be several-fold. One of these is a protective action against nigrostriatal damage. This possibility stems from the results of epidemiological studies that consistently demonstrate an inverse correlation between tobacco use and Parkinson's disease. This reduced incidence of Parkinson's disease has been attributed to the nicotine in tobacco products, at least in part, based on experimental work showing a protective effect of nicotine against toxic insults. Second, several studies suggest a symptomatic effect of nicotine in Parkinson's disease, although effects are small and somewhat variable. Third, recent data in nonhuman primates show that nicotine attenuates levodopa-induced dyskinesias, a debilitating side effect that develops in the majority of patients on levodopa therapy. Collectively, these observations suggest that nicotine or CNS selective nicotinic receptor ligands hold promise for Parkinson's disease therapy to reduce disease progression, improve symptoms, and/or decrease levodopa-induced dyskinesias.

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Prior work from the authors' laboratory indicates that nicotine lowers L-DOPA-induced AIMs across multiple parkinsonian animal models.
“Recent studies from our laboratory show that nicotine treatment reduces L-DOPA-induced AIMs in several different parkinsonian animal models (Quik et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Quik et al., 2008
α4β2* nAChRs in the striatum are 80% localized postsynaptically on GABAergic neurons where they modulate GABA release and 20% presynaptically on dopaminergic terminals involved in regulating dopamine release.
“In addition, they are present in the striatum, with 80% localized postsynaptically on GABAergic neurons where they modulate GABA release and 20% presynaptically on dopaminergic terminals that are involved in regulating dopamine release (Grady et al., 2007;Quik et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Quik et al., 2008
α6β2* nAChRs localized to catecholaminergic neurons may also be relevant for the observed effects of nicotine on L-DOPA-induced AIMs.
“The ␣6␤2* nAChRs localized to catecholaminergic neurons may also be of relevance for the observed effects of nicotine on L-DOPA-induced AIMs (Grady et al., 2007;Quik et al., 2008).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Quik et al., 2008

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Nicotine protects rat brain mitochondria against experimental injuries
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Stimulation of non-α7 nicotinic receptors partially protects dopaminergic neurons from 1-methyl-4-phenylpyridinium-induced toxicity in culture
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THE DOPAMINERGIC NIGROSTRIATAL SYSTEMAND PARKINSON'S DISEASE
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Decaffeinated Coffee and Nicotine-Free Tobacco Provide Neuroprotection in Drosophila Models of Parkinson's Disease through an NRF2-Dependent Mechanism
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Differential Involvement of D1 and D2 Dopamine Receptors in L-DOPA-Induced Angiogenic Activity in a Rat Model of Parkinson's Disease
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Parkinson’s Disease is Predominantly a Genetic Disease
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Authors: Quik, M., O'Leary, K., & Tanner, C. M.
Affiliations: Parkinson's Institute and Clinical Center (US)
Corresponding author: Quik, Maryka
ORCID: Tanner, Caroline M.
Venue: Movement Disorders
Publisher: Wiley
Published: 2008-08-05
Volume: 23
Issue: 12
Pages: 1641-1652
ISSN: 0885-3185 (ISSN-L)
1531-8257
DOI: 10.1002/mds.21900
PMC: PMC4430096
OpenAlex: W2038311990
Cited by: 154
References: 137
Citations by year: 2026: 12 · 2025: 15 · 2024: 7 · 2023: 8 · 2022: 8 · 2021: 10 · 2020: 6 · 2019: 7 · 2018: 5 · 2017: 6 · 2016: 6 · 2015: 3 · 2014: 8 · 2013: 10 · 2012: 9
FWCI: 1.68
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Movement Disorders (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Neurological Disorders and Stroke (NS 34886, R01NS047162, NS42091, NS40467, R01NS034886, R01NS059910, R01NS040467, R01NS042091)
National Institute of Environmental Health Sciences (U54ES012077, ES 012077)
Topics: Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords: nicotine, Parkinson's disease, nicotinic acetylcholine receptors, tobacco use, levodopa-induced dyskinesia, symptomatic treatment, disease progression
MeSH terms: Animals, Antiparkinson Agents, Humans, Nicotine, Parkinson Disease

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Nicotine and Parkinson's disease: implications for therapy

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