Evidence map›Paper›PMID 25672665›Full record

ReviewCellular and molecular neurobiology2015

The neuronal nitric oxide synthase (nNOS) gene and neuroprotection against alcohol toxicity.

Bahri Karaçay, Daniel J Bonthius

Abstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  6. Nitrergic Enteric Neurons in Health and Disease-Focus on Animal Models.International journal of molecular sciences · 2019
    Review
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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 1 institution in 1 country.

Bahri KaraçayDepartment of Pediatrics, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, USA.
Daniel J Bonthius
University of Iowa · US

Funding

NO-mediated neuroprotection against alcohol: mechanism and potential therapyR01AA021465 · NIAAA · UNIVERSITY OF IOWA · PI BONTHIUS, DANIEL J. · 2013 to 2017
$1.7M
Role of MicroRNAs in Fetal Alcohol SyndromeR21AA018710 · NIAAA · UNIVERSITY OF IOWA · PI BONTHIUS, DANIEL J., KARACAY, BAHRI · 2010 to 2011
$404k
Prevention of Alcohol Neurotoxicity by PDE4 InhibitorR21AA018711 · NIAAA · UNIVERSITY OF IOWA · PI BONTHIUS, DANIEL J., KARACAY, BAHRI · 2010 to 2011
$404k
Regulation of Microglial Responses to Alcohol and Alcohol-Induced NeurodegeneratiR21AA018823 · NIAAA · UNIVERSITY OF IOWA · PI DAILEY, MICHAEL E · 2009 to 2010
$391k
Maturation dependent neuroprotection against alcoholR21AA015747 · NIAAA · UNIVERSITY OF IOWA · PI KARACAY, BAHRI · 2005 to 2006
$382k
NIAAA NIH HHS AA015747-01NIAAA NIH HHS AA018711NIAAA NIH HHS AA018823-91NIAAA NIH HHS AA021465-02NIAAA NIH HHS R01 AA021465NIAAA NIH HHS R21 AA015747NIAAA NIH HHS R21 AA018710NIAAA NIH HHS R21 AA018711NIAAA NIH HHS R21 AA018823
6 · The paper itself

Abstract

When a mother abuses alcohol during pregnancy, the offspring can suffer a myriad of abnormalities, collectively known as fetal alcohol spectrum disorder (FASD). Foremost among these abnormalities is central nervous system dysfunction, which commonly manifests itself as mental retardation, clumsiness, hyperactivity, and poor attention span. These behavior problems are due, in large part, to alcohol-induced neuronal losses in the developing fetal brain. However, not all fetuses are equally affected by maternal alcohol consumption during pregnancy. While some fetuses are severely affected and develop hallmarks of FASD later in life, others exhibit no evident neuropathology or behavioral abnormalities. This variation is likely due, at least in part, to differences in fetal genetics. This review focuses on one particular gene, neuronal nitric oxide synthase, whose mutation worsens alcohol-induced neuronal death, both in vitro and in vivo. In addition, ectopic expression of the neuronal nitric oxide synthase gene protects neurons against alcohol toxicity. The gene encodes an enzyme that produces nitric oxide (NO), which facilitates the protective effects of neuronal growth factors and which underlies the ability of neurons to resist alcohol toxicity as they mature. Nitric oxide exerts its protective effects against alcohol via a specific signaling pathway, the NO-cGMP-PKG pathway. Pharmacologic manipulation of this pathway could be of therapeutic use in preventing or ameliorating FASD.

Indexed as

AlcoholsAnimalsHumansNeuroprotectionNeuroprotective AgentsNitric OxideNitric Oxide Synthase Type IN-MethylaspartateAlcoholsNeuroprotective AgentsNitric OxideNitric Oxide Synthase Type IN-Methylaspartate

Identifiers

PMID25672665
PMCPMC4380853
OpenAlexW2006468979

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.