Evidence map›Paper›PMID 16906354›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2007

Nicotinic receptor agonists as neuroprotective/neurotrophic drugs. Progress in molecular mechanisms.

G Mudo, N Belluardo, K Fuxe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Smoking and increased Alzheimer's disease risk: a review of potential mechanisms.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Involvement ofFrontiers in molecular biosciences · 2020
    Article
  8. Retinal correlates of psychiatric disorders.Therapeutic advances in chronic disease · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Smoking-Relevant Nicotine Concentration Attenuates the Unfolded Protein Response in Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Review
  18. Article
  19. In vivo PET imaging of the α4β2 nicotinic acetylcholine receptor as a marker for brain inflammation after cerebral ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  20. Article
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 2 countries.

G MudoDepartment of Experimental Medicine, Section of Human Physiology, University of Palermo, Palermo, Italy. g.mudo@unipa.it
N Belluardo
K Fuxe
University of Palermo · ITKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present work we reviewed recent advances concerning neuroprotective/neurotrophic effects of acute or chronic nicotine exposure, and the signalling pathways mediating these effects, including mechanisms implicated in nicotine addiction and nAChR desensitization. Experimental and clinical data largely indicate long-lasting effects of nicotine and nicotinic agonists that imply a neuroprotective/neurotrophic role of nAChR activation, involving mainly alpha7 and alpha4beta2 nAChR subtypes, as evidenced using selective nAChR agonists. Compounds interacting with neuronal nAChRs have the potential to be neuroprotective and treatment with nAChR agonists elicits long-lasting neurotrophic effects, e.g. improvement of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Nicotine addiction, which is mediated by interaction with nACh receptors, is believed to involve the modification of signalling cascades that modulate synaptic plasticity and gene expression. Desensitization, in addition to protecting cells from uncontrolled excitation, is recently considered as a form of signal plasticity. nAChR can generate these longe-lasting effects by elaboration of complex intracellular signals that mediate medium to long-term events crucial for neuronal maintenance, survival and regeneration. Although a comprehensive survey of the gene-based molecular mechanisms that underlie nicotine effects has yet not been performed a growing amount of data is beginning to improve our understanding of signalling mechanisms that lead to neurotrophic/neuroprotective responses. Evidence for an involvement of the fibroblast growth factor-2 gene in nAChR mechanisms mediating neuronal survival, trophism and plasticity has been obtained. However, more work is needed to establish the mechanisms involved in the effects of nicotinic receptor subtype activation from cognition-enhancing and neurotrophic effects to smoking behaviour and to determine more precisely the therapeutic objectives in potential nicotinic drug treatments of neurodegenerative diseases.

Indexed as

AnimalsBrainHumansNerve Growth FactorsNeurodegenerative DiseasesNeuronal PlasticityNeuroprotective AgentsNicotinic AgonistsReceptors, NicotinicSignal TransductionTobacco Use DisorderNerve Growth FactorsNeuroprotective AgentsNicotinic AgonistsReceptors, Nicotinic

Identifiers

PMID16906354
OpenAlexW2009734654

What OpenQuestion holds

Textmetadata
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.