Evidence map›Paper›PMID 28694481›Full record

ArticleScientific reports2017

Mechanisms underlying neuro-inflammation and neurodevelopmental toxicity in the mouse neocortex following prenatal exposure to ethanol.

Munekazu Komada, Nao Hara, Satoko Kawachi, Kota Kawachi, Nao Kagawa, Tetsuji Nagao, Yayoi Ikeda

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
10.2field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. EpiBrain: the brain's epigenetic landscape in a snapshot.bioRxiv : the preprint server for biology · 2026
    Article
  4. Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Behavioral changes inFrontiers in neuroscience · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice.Frontiers in cell and developmental biology · 2022
    Article
  17. Review
  18. Review
  19. Review
  20. Review
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

7 authors at 2 institutions in 1 country.

Munekazu KomadaDepartment of Anatomy, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, Aichi, 464-8650, Japan. komada@dpc.agu.ac.jp.
Nao HaraDepartment of Life Science, Kindai University, 3-4-1 Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Satoko KawachiDepartment of Life Science, Kindai University, 3-4-1 Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Kota KawachiDepartment of Life Science, Kindai University, 3-4-1 Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Nao KagawaDepartment of Life Science, Kindai University, 3-4-1 Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Tetsuji NagaoDepartment of Life Science, Kindai University, 3-4-1 Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Yayoi IkedaDepartment of Anatomy, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, Aichi, 464-8650, Japan.
Kindai University · JPAichi Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fetal alcohol spectrum disorders (FASD) constitute a wide range of disorders that arise from prenatal exposure to ethanol (EtOH). However, detailed reports regarding the adverse effects of prenatal EtOH exposure on neocortical morphology and its underlying pathogenic mechanisms are limited. In the present study, we aimed to characterize the anatomical abnormalities of neocortical development and their correlation with microglial properties and neuro-inflammation in a mouse model of FASD. We evaluated the development and maturation of the neocortex in ICR mice prenatally exposed to 25% (w/v) EtOH using histological and molecular analyses. Reduced proliferation and excessive cell death were observed in the dorsal telencephalon. Abnormal neuronal distribution, layer formation, and dopaminergic neuronal projections were observed in the neocortex. Disruption of microglial differentiation (M1/M2 microglial ratio) and abnormal expression of pro-inflammatory and neurotrophic factors were induced, and these abnormalities were ameliorated by co-treatment with an anti-inflammatory drug (pioglitazone). FASD model mice displayed histological abnormalities, microglial abnormalities, and neuro-inflammation in both the embryonic and newborn stages. Thus, anti-inflammatory therapeutics may provide a novel preventive approach for the treatment of FASD.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsCell ProliferationCell SurvivalCytokinesDopaminergic NeuronsEthanolFemaleFetal Alcohol Spectrum DisordersInflammationInflammation MediatorsMiceMicrogliaNeocortexNeurodevelopmental DisordersNeurogenesisCytokinesEthanolInflammation Mediators

Identifiers

PMID28694481
PMCPMC5504035
OpenAlexW2726842926

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.