Evidence map›Paper›PMID 17554626›Full record

ReviewCellular and molecular neurobiology2007

Cognitive deficits in schizophrenia: focus on neuronal nicotinic acetylcholine receptors and smoking.

Enrique L M Ochoa, Jose Lasalde-Dominicci

Abstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 63 citations in OpenAlex.

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  13. Newer antipsychotics and upcoming molecules for schizophrenia.European journal of clinical pharmacology · 2013
    Review
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  19. Selective α4β2 nicotinic acetylcholine receptor agonists target epigenetic mechanisms in cortical GABAergic neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    Article
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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

2 authors at 2 institutions in 2 countries.

Enrique L M OchoaDepartment of Psychiatry, University of California at Davis, 2230 Stockton Boulevard, Sacramento, CA 95817, USA. elochoa@ucdavis.edu
Jose Lasalde-Dominicci
University of California, Davis · USUniversity of Puerto Rico System · PR

Funding

X-RAY STUDY OF SYNTHETIC OXYGEN CARRIERS RELATED TO BIOLOGICAL SYSTEMSS06GM008102 · NIGMS · UNIVERSITY OF PUERTO RICO RIO PIEDRAS · PI ARCE, RAFAEL · 1989 to 2008
$23.8M
The Role of Sensory Input to Mammalian Locomotion After the Loss of supraspinal.P20GM103642 · NIGMS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI LASALDE-DOMINICCI, JOSE ANTONIO · 2013 to 2023
$20.6M
LIPID INTERACTIONS ALTER ACETYLCHOLINE RECEPTORR01GM056371 · NIGMS · UNIVERSITY OF PUERTO RICO RIO PIEDRAS · PI LASALDE-DOMINICCI, JOSE A · 1997 to 2005
$1.3M
NIGMS NIH HHS 2R01GM56371-10NIGMS NIH HHS P20 GM103642NIGMS NIH HHS R01 GM056371NIGMS NIH HHS S06 GM008102
6 · The paper itself

Abstract

Patients with schizophrenia present with deficits in specific areas of cognition. These are quantifiable by neuropsychological testing and can be clinically observable as negative signs. Concomitantly, they self-administer nicotine in the form of cigarette smoking. Nicotine dependence is more prevalent in this patient population when compared to other psychiatric conditions or to non-mentally ill people. The target for nicotine is the neuronal nicotinic acetylcholine receptor (nAChR). There is ample evidence that these receptors are involved in normal cognitive operations within the brain. This review describes neuronal nAChR structure and function, focusing on both cholinergic agonist-induced nAChR desensitization and nAChR up-regulation. The several mechanisms proposed for the nAChR up-regulation are examined in detail. Desensitization and up-regulation of nAChRs may be relevant to the physiopathology of schizophrenia. The participation of several subtypes of neuronal nAChRs in the cognitive processing of non-mentally ill persons and schizophrenic patients is reviewed. The role of smoking is then examined as a possible cognitive remediator in this psychiatric condition. Finally, pharmacological strategies focused on neuronal nAChRs are discussed as possible therapeutic avenues that may ameliorate the cognitive deficits of schizophrenia.

Indexed as

CognitionCognition DisordersHumansNicotineNicotinic AgonistsReceptors, NicotinicSchizophreniaSmokingNicotineNicotinic AgonistsReceptors, Nicotinic

Identifiers

PMID17554626
PMCPMC4676572
OpenAlexW2136546688

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.