Evidence map›Paper›PMID 23871750›Full record

ReviewProgress in neuro-psychopharmacology & biological psychiatry2014

Neurocognitive endophenotypes in schizophrenia: modulation by nicotinic receptor systems.

Kristen M Mackowick, Mera S Barr, Victoria C Wing, Rachel A Rabin, Clairelaine Ouellet-Plamondon, Tony P George

Abstract readReview
In one paragraph

Review in Progress in neuro-psychopharmacology & biological psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Kristen M MackowickThe Institute of Medical Sciences (IMS), University of Toronto, Toronto, Ontario Canada; Schizophrenia Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario Canada.
Mera S BarrSchizophrenia Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario Canada.
Victoria C WingSchizophrenia Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario Canada.
Rachel A RabinThe Institute of Medical Sciences (IMS), University of Toronto, Toronto, Ontario Canada; Schizophrenia Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario Canada.
Clairelaine Ouellet-PlamondonSchizophrenia Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario Canada.
Tony P GeorgeThe Institute of Medical Sciences (IMS), University of Toronto, Toronto, Ontario Canada; Schizophrenia Division, Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario Canada; Faculty of Medicine, University of Toronto, Toronto, Ontario Canada; Division of Brain and Therapeutics, Department of Psychiatry, University of Toronto, Toronto, Ontario Canada. Electronic address: tony.george@camh.ca.
Centre for Addiction and Mental Health · CAUniversity of Toronto · CA

Funding

Nicotinic Receptors and Cog Function in SchizophreniaR01DA014039 · NIDA · YALE UNIVERSITY · PI GEORGE, TONY P · 2001 to 2003
$627k
Translational Studies on Smoking in SchizophreniaK02DA016611 · NIDA · YALE UNIVERSITY · PI GEORGE, TONY P · 2004 to 2006
$307k
CIHR MOP#115145NIDA NIH HHS K02 DA016611NIDA NIH HHS K02-DA-016611NIDA NIH HHS R01 DA014039
6 · The paper itself

Abstract

Cigarette smoking is the leading preventable cause of death in the Western world, with a considerably higher prevalence observed in schizophrenia compared to the general population. Despite the negative health consequences of smoking heavily, it has been proposed that individuals with schizophrenia may maintain smoking behaviors to remediate symptoms associated with the disorder. Neurocognitive deficits are a core feature of schizophrenia and are present in approximately 80% of patients. Further, these deficits constitute an endophenotype of schizophrenia, as they are stable across disease phases, and are heritable. The neurocognitive deficits that are present in schizophrenia are especially debilitating, since they are associated with poor clinical and functional outcomes and community integration. Interestingly, these deficits may also constitute a vulnerability factor towards the initiation and maintenance of tobacco use. Contributing to the potential shared vulnerability between schizophrenia and tobacco dependence is a dysregulation of the nicotinic acetylcholine receptor (nAChR) system. Pre-clinical evidence has shown that nicotine affects several neurotransmitter systems, including dopamine (DA), glutamate, and γ-aminobutyric acid (GABA), and certain neuropsychological deficits associated with these neurotransmitters (reaction time, spatial working memory, sustained attention, and sensory gating) are improved after nicotine administration in patients with schizophrenia. These positive effects on neurocognition appear to be more pronounced in smokers with schizophrenia, and may be an important mechanism that explains the co-morbidity of schizophrenia and tobacco dependence.

Indexed as

EndophenotypesAnimalsCognition DisordersHumansNicotineReceptors, NicotinicSchizophreniaTobacco Use DisorderNicotineReceptors, NicotinicCognitionEndophenotypeNicotineNicotinic acetylcholine receptorsSchizophreniaTobacco

Identifiers

PMID23871750
PMCPMC3851927
OpenAlexW1986682925

What OpenQuestion holds

Textmetadata
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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.