Evidence map›Paper›PMID 22693036›Full record

ReviewMovement disorders : official journal of the Movement Disorder Society2012

Nicotine as a potential neuroprotective agent for Parkinson's disease.

Maryka Quik, Xiomara A Perez, Tanuja Bordia

Open access · greenAbstract readReview
In one paragraph

Review in Movement disorders : official journal of the Movement Disorder Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 5 pooled it
9.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

126 citing papers in PubMed, 5 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Pooled it
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  5. Effect of nicotine on L-dopa-induced dyskinesia in animal models of Parkinson's disease: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
    Pooled it
  6. Trial
  7. Article
  8. Review
  9. Genetic and Proteomic Investigation of the Smoking-Parkinson's Disease Association.medRxiv : the preprint server for health sciences · 2026
    Article
  10. Article
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  18. "Unraveling the role ofReceptors (Basel, Switzerland) · 2025
    Article
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  20. Article

66 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Maryka QuikCenter for Health Sciences, SRI International, Menlo Park, California, USA. maryka.quik@sri.com
Xiomara A Perez
Tanuja Bordia
SRI International · USOklahoma State University Center for Health Sciences · US

Funding

Mechanisms of nicotine-mediated decrease in L-dopa induced-dyskinesiasR01NS059910 · NINDS · SRI INTERNATIONAL · PI QUIK, MARYKA · 2009 to 2013
$3.7M
Nicotinic receptors as molecular targets to reduce L-dopa-induced dyskinesias inR21NS065851 · NINDS · SRI INTERNATIONAL · PI QUIK, MARYKA · 2010 to 2011
$485k
NINDS NIH HHS NS59910NINDS NIH HHS NS65851NINDS NIH HHS R01 NS059910NINDS NIH HHS R21 NS065851
6 · The paper itself

Abstract

Converging research efforts suggest that nicotine and other drugs that act at nicotinic acetylcholine receptors (nAChRs) may be beneficial in the management of Parkinson's disease. This idea initially stemmed from the results of epidemiological studies that demonstrated that smoking is associated with a decreased incidence of Parkinson's disease. The subsequent finding that nicotine administration protected against nigrostriatal damage in parkinsonian animal models led to the idea that nicotine in tobacco products may contribute to this apparent protective action. Nicotine most likely exerts its effects by interacting at nAChRs. Accumulating research indicates that multiple subtypes containing nAChRs, including α4β2, α6β2, and/or α7, may be involved. Stimulation of nAChRs initially activates various intracellular transduction pathways primarily via alterations in calcium signaling. Consequent adaptations in immune responsiveness and trophic factors may ultimately mediate nicotine's ability to reduce/halt the neuronal damage that arises in Parkinson's disease. In addition to a potential neuroprotective action, nicotine also has antidepressant properties and improves attention/cognition. Altogether, these findings suggest that nicotine and nAChR drugs represent promising therapeutic agents for the management of Parkinson's disease.

Indexed as

Neuroprotective AgentsAnimalsCorpus StriatumDisease Models, AnimalHumansNicotineNicotinic AgonistsParkinson DiseaseParkinson Disease, SecondaryReceptors, NicotinicSignal TransductionSmokingSubstantia NigraNeuroprotective AgentsNicotineNicotinic AgonistsReceptors, Nicotinic

Identifiers

PMID22693036
PMCPMC3685410
OpenAlexW2030764484

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.