Evidence map›Paper›PMID 29106518›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2018

Prenatal Ethanol Exposure and Neocortical Development: A Transgenerational Model of FASD.

Charles W Abbott, David J Rohac, Riley T Bottom, Sahil Patadia, Kelly J Huffman

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2018. 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
11.8field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Epigenetic Inheritance and Transgenerational Environmental Justice.The Yale journal of biology and medicine · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Article
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  18. Review
  19. Article
  20. Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice.Frontiers in cell and developmental biology · 2022
    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

5 authors at 1 institution in 1 country.

Charles W AbbottDepartment of Psychology and Interdepartmental Neuroscience Program, University of California, Riverside, 900 University Ave. Riverside, CA, USA.
David J RohacDepartment of Psychology and Interdepartmental Neuroscience Program, University of California, Riverside, 900 University Ave. Riverside, CA, USA.
Riley T BottomDepartment of Psychology and Interdepartmental Neuroscience Program, University of California, Riverside, 900 University Ave. Riverside, CA, USA.
Sahil PatadiaDepartment of Psychology and Interdepartmental Neuroscience Program, University of California, Riverside, 900 University Ave. Riverside, CA, USA.
Kelly J HuffmanDepartment of Psychology and Interdepartmental Neuroscience Program, University of California, Riverside, 900 University Ave. Riverside, CA, USA.
University of California, Riverside · US

Funding

Prenatal ethanol exposure & neocortex, functional org. & gene expressionR03AA021545 · NIAAA · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI HUFFMAN, KELLY · 2012 to 2013
$147k
NIAAA NIH HHS R03 AA021545
6 · The paper itself

Abstract

Fetal Alcohol Spectrum Disorders, or FASD, represent a range of adverse developmental conditions caused by prenatal ethanol exposure (PrEE) from maternal consumption of alcohol. PrEE induces neurobiological damage in the developing brain leading to cognitive-perceptual and behavioral deficits in the offspring. Alcohol-mediated alterations to epigenetic function may underlie PrEE-related brain dysfunction, with these changes potentially carried across generations to unexposed offspring. To determine the transgenerational impact of PrEE on neocortical development, we generated a mouse model of FASD and identified numerous stable phenotypes transmitted via the male germline to the unexposed third generation. These include alterations in ectopic intraneocortical connectivity, upregulation of neocortical Rzrβ and Id2 expression accompanied by both promoter hypomethylation of these genes and decreased global DNA methylation levels. DNMT expression was also suppressed in newborn PrEE cortex, providing further insight into how ethanol perturbs DNA methylation leading to altered regulation of gene transcription. These PrEE-induced, transgenerational phenotypes may be responsible for cognitive, sensorimotor, and behavioral deficits seen in humans with FASD. Thus, understanding the possible epigenetic mechanisms by which these phenotypes are generated may reveal novel targets for therapeutic intervention of FASD and lead to advances in human health.

Indexed as

AnimalsAnimals, NewbornBody WeightCentral Nervous System DepressantsDevelopmental DisabilitiesDisease Models, AnimalDNA MethylationEpigenomicsEthanolFemaleFetal Alcohol Spectrum DisordersMaleMiceMood DisordersMotor ActivityNeocortexCentral Nervous System DepressantsEthanolRNA, Messenger

Identifiers

PMID29106518
PMCPMC6041800
OpenAlexW2732741185

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.