Evidence map›Paper›PMID 23763370›Full record

ArticleAlcoholism, clinical and experimental research2013

Low-dose thyroxine attenuates autism-associated adverse effects of fetal alcohol in male offspring's social behavior and hippocampal gene expression.

Elif Tunc-Ozcan, Timothy M Ullmann, Pradeep K Shukla, Eva E Redei

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
8.3field-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

30 citing papers in PubMed, 38 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Elif Tunc-OzcanDepartment of Psychiatry and Behavioral Sciences, The Asher Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Timothy M Ullmann
Pradeep K Shukla
Eva E Redei
Northwestern University · US

Funding

Prenatal Alcohol;Hormone-Regulated Genes &BehaviorR01AA013452 · NIAAA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI REDEI, EVA E · 2002 to 2010
$2.3M
Epigenetic Consequences of Prenatal Alcohol ExposureR01AA017978 · NIAAA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI REDEI, EVA E · 2009 to 2014
$1.8M
NIAAA NIH HHS AA013452NIAAA NIH HHS AA017978NIAAA NIH HHS R01 AA013452NIAAA NIH HHS R01 AA017978
6 · The paper itself

Abstract

backgroundFetal alcohol spectrum disorder (FASD) is characterized by neurodevelopmental anomalies manifesting in cognitive and behavioral deficits in the offspring with diverse severities. Social behavior is affected in FASD, and these deficits overlap with those of autism spectrum disorder (ASD). Identifying some of the molecular characteristics related to ASD in an animal model of FASD could ultimately provide details on the underlying molecular mechanisms of both disorders that could lead to novel treatments.

methodsPregnant Sprague-Dawley rats received the following diets: control (C; ad libitum standard laboratory chow), nutritional control pair-fed (PF), ethanol (EtOH), or an EtOH diet supplemented with 0.3, 1.5, or 7.5 mg thyroxine (T4)/l in the diet. Social behavior and memory were tested in the adult offspring. Plasma total T4, free T3 (fT3), and thyroid-stimulating hormone (TSH) levels were measured. Hippocampal expression of Gabrb3, Ube3a, Nr2b, Rasgrf1, and Dio3 were measured by RT-qPCR and protein levels of Mecp2 and Slc25a12 by Western blotting.

resultsAdult male offspring of EtOH dams showed elevated fT3 and low TSH levels. Adult male, but not female, offspring of EtOH dams exhibited social behavior and memory deficits. Expression of autism candidates, Gabrb3, Ube3a, Mecp2, and Slc25a12, was significantly increased in the hippocampus of male offspring of EtOH dams. Hippocampal Nr2b and Dio3 were also increased, while Rasgrf1 was decreased in the same population. Peripheral thyroid function, social behavioral deficits, and altered expression of the above genes were normalized by simultaneous administration of 0.3 mg/l T4 in the EtOH diet.

conclusionsOur data suggest that social interaction deficits of FASD share molecular mechanism with ASD by showing altered hippocampal expression of several ASD candidate genes. Social interaction deficits as well as the gene expression changes in the offspring of EtOH-consuming dams can be reversed by low dose of thyroid hormone supplementation to the mothers.

Indexed as

AnimalsAutistic DisorderEthanolFemaleFetal Alcohol Spectrum DisordersHippocampusMalePregnancyPrenatal Exposure Delayed EffectsRatsRats, Sprague-DawleySocial BehaviorThyroxineEthanolThyroxineAutism Spectrum DisordersFetal Alcohol Spectrum DisordersSocial InteractionSocial MemoryThyroxine

Identifiers

PMID23763370
PMCPMC3805686
OpenAlexW2147708794

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.