Evidence map›Paper›PMID 28518477›Full record

ArticleGlia2017

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorder.

Jessie Newville, Carlos Fernando Valenzuela, Lu Li, Lauren L Jantzie, Lee Anna Cunningham

Open access · greenAbstract read
In one paragraph

Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
8.5field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  5. Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026
    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

5 authors at 1 institution in 1 country.

Jessie NewvilleDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.ORCID 0000-0002-8590-7968
Carlos Fernando ValenzuelaDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Lu LiDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Lauren L JantzieDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.ORCID 0000-0002-5410-3553
Lee Anna CunninghamDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
University of New Mexico · US

Funding

University of New Mexico (UNM) Center for Brain Recovery and RepairP20GM109089 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI SHUTTLEWORTH, CLAUDE W · 2015 to 2024
$22.7M
Understanding neurophysiological deficits in response inhibition in children with FASDP50AA022534 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2014 to 2026
$21.5M
NIAAA NIH HHS P50 AA022534NIGMS NIH HHS P20 GM109089
6 · The paper itself

Abstract

Alcohol exposure during central nervous system (CNS) development can lead to fetal alcohol spectrum disorder (FASD). Human imaging studies have revealed significant white matter (WM) abnormalities linked to cognitive impairment in children with FASD; however, the underlying mechanisms remain unknown. Here, we evaluated both the acute and long-term impacts of alcohol exposure on oligodendrocyte number and WM integrity in a third trimester-equivalent mouse model of FASD, in which mouse pups were exposed to alcohol during the first 2 weeks of postnatal development. Our results demonstrate a 58% decrease in the number of mature oligodendrocytes (OLs) and a 75% decrease in the number of proliferating oligodendrocyte progenitor cells (OPCs) within the corpus callosum of alcohol-exposed mice at postnatal day 16 (P16). Interestingly, neither mature OLs nor OPCs derived from the postnatal subventricular zone (SVZ) were numerically affected by alcohol exposure, indicating heterogeneity in susceptibility based on OL ontogenetic origin. Although mature OL and proliferating OPC numbers recovered by postnatal day 50 (P50), abnormalities in myelin protein expression and microstructure within the corpus callosum of alcohol-exposed subjects persisted, as assessed by western immunoblotting of myelin basic protein (MBP; decreased expression) and MRI diffusion tensor imaging (DTI; decreased fractional anisotropy). These results indicate that third trimester-equivalent alcohol exposure leads to an acute, albeit recoverable, decrease in OL lineage cell numbers, accompanied by enduring WM injury. Additionally, our finding of heterogeneity in alcohol susceptibility based on the developmental origin of OLs may have therapeutic implications in FASD and other disorders of WM development.

Indexed as

Pregnancy Trimester, ThirdAnimalsCell ProliferationCentral Nervous System DepressantsDisease Models, AnimalEthanolFemaleFetal Alcohol Spectrum DisordersLeukoencephalopathiesLuminescent ProteinsMaleMiceMice, Inbred C57BLMice, TransgenicMyelin Basic ProteinNestinCentral Nervous System DepressantsEthanolLuminescent ProteinsMyelin Basic ProteinNes protein, mouseNestinReceptor, Platelet-Derived Growth Factor alphacorpus callosumdiffusion tensor imagingmyelin basic proteinoligodendrogenesissubventricular zone

Identifiers

PMID28518477
PMCPMC5497771
OpenAlexW2616259342

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.