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Teratogenicity

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...

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Related Experiment Video

Updated: Jun 25, 2025

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

Published on: August 5, 2017

Risk and Resilience Variants in the Retinoic Acid Metabolic and Developmental Pathways Associated with Risk of FASD

Leo McKay¹, Berardino Petrelli¹, Molly Pind¹

¹Department of Biochemistry & Medical Genetics, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E 0J9, Canada.

|May 24, 2024

Summary

Fetal Alcohol Spectrum Disorder (FASD) is linked to prenatal alcohol exposure (PAE). Genetic variants in alcohol metabolism and retinoic acid (RA) pathways may explain FASD risk and resilience.

Keywords:

FASD FASD risk outcomes PAE biomarkers fetal alcohol spectrum disorder genetic variants prenatal alcohol exposure rare neurodevelopmental disorders retinoic acid whole exome sequencing

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Area of Science:

Neuroscience
Genetics
Developmental Biology

Background:

Fetal Alcohol Spectrum Disorder (FASD) is a prevalent neurodevelopmental disorder in North America, affecting 2-5% of the population.
Prenatal alcohol exposure (PAE) is the primary cause, but the underlying genetic factors remain largely unknown.
Retinoic acid (RA) signaling is crucial for development and may be disrupted by PAE.

Purpose of the Study:

To investigate the genetic underpinnings of FASD by analyzing genes involved in RA metabolism and signaling pathways.
To identify genetic variants associated with risk and resilience in individuals diagnosed with FASD.
To explore the role of PAE-induced RA deficiency in FASD etiology.

Main Methods:

Candidate gene approach using whole exome sequencing data from 23 individuals with FASD.
Analysis of genetic variants in alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes.
Examination of variants in RA-regulated developmental pathway genes (e.g., SHH, WNT) and genes associated with comorbid neurodevelopmental disorders.

Main Results:

Identified risk and resilience alleles in ADH and ALDH genes, suggesting PAE disrupts RA production via alcohol metabolism.
Found significant variants in RA-regulated developmental pathways, including SHH and WNT.
Detected variants in genes linked to rare neurodevelopmental disorders with FASD comorbidities (STRA6, SOX9, FDG1, TBX1).

Conclusions:

PAE-induced RA deficiency is a significant etiological factor in FASD.
Genetic variants in RA metabolic and developmental pathways may serve as biomarkers for FASD risk and outcomes.
Further research is warranted to validate these findings in larger cohorts.