Evidence map›Paper›PMID 25175861›Full record

ReviewInternational review of neurobiology2014

Fetal alcohol spectrum disorders and neuroimmune changes.

Paul D Drew, Cynthia J M Kane

Abstract readReview
In one paragraph

Review in International review of neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
53.4field-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

54 citing papers in PubMed, 77 citations in OpenAlex.

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  18. Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum.International journal of environmental research and public health · 2021
    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 2 institutions in 1 country.

Paul D DrewDepartment of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Cynthia J M KaneDepartment of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. Electronic address: kanecynthiaj@uams.edu.
University of Arkansas for Medical Sciences · USUniversity of Arkansas Medical Center · US

Funding

Microglia modulate ethanol impact on CNS development.R01AA018834 · NIAAA · UNIV OF ARKANSAS FOR MED SCIS · PI KANE, CYNTHIA J. · 2009 to 2013
$1.6M
Mechanisms of Ethanol-Induced Neuroinflammation and NeurodegenerationRC1AA019108 · NIAAA · UNIV OF ARKANSAS FOR MED SCIS · PI DREW, PAUL D · 2009 to 2010
$1000k
Effects of Alcohol on Microglia and Innate ImmunityR21AA018839 · NIAAA · UNIV OF ARKANSAS FOR MED SCIS · PI DREW, PAUL D · 2009 to 2010
$397k
NIAAA NIH HHS AA18834NIAAA NIH HHS AA18839NIAAA NIH HHS AA19108NIAAA NIH HHS R01 AA018834NIAAA NIH HHS R21 AA018839NIAAA NIH HHS RC1 AA019108
6 · The paper itself

Abstract

The behavioral consequences of fetal alcohol spectrum disorders (FASD) are serious and persist throughout life. The causative mechanisms underlying FASD are poorly understood. However, much has been learned about FASD from human structural and functional studies as well as from animal models, which have provided a greater understanding of the mechanisms underlying FASD. Using animal models of FASD, it has been recently discovered that ethanol induces neuroimmune activation in the developing brain. The resulting microglial activation, production of proinflammatory molecules, and alteration in expression of developmental genes are postulated to alter neuron survival and function and lead to long-term neuropathological and cognitive defects. It has also been discovered that microglial loss occurs, reducing microglia's ability to protect neurons and contribute to neuronal development. This is important, because emerging evidence demonstrates that microglial depletion during brain development leads to long-term neuropathological and cognitive defects. Interestingly, the behavioral consequences of microglial depletion and neuroimmune activation in the fetal brain are particularly relevant to FASD. This chapter reviews the neuropathological and behavioral abnormalities of FASD and delineates correlates in animal models. This serves as a foundation to discuss the role of the neuroimmune system in normal brain development, the consequences of microglial depletion and neuroinflammation, the evidence of ethanol induction of neuroinflammatory processes in animal models of FASD, and the development of anti-inflammatory therapies as a new strategy for prevention or treatment of FASD. Together, this knowledge provides a framework for discussion and further investigation of the role of neuroimmune processes in FASD.

Indexed as

AnimalsFetal Alcohol Spectrum DisordersHumansNeuroimmunomodulationAlcoholBrain developmentChemokineCytokineFetal alcohol spectrum disordersMicrogliaNeuroimmuneNeuroinflammationTherapeuticsToll-like receptor

Identifiers

PMID25175861
PMCPMC4387770
OpenAlexW2411789234

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.