4.4 Review

Biobehavioral Markers of Adverse Effect in Fetal Alcohol Spectrum Disorders

Journal

NEUROPSYCHOLOGY REVIEW
Volume 21, Issue 2, Pages 148-166

Publisher

SPRINGER
DOI: 10.1007/s11065-011-9169-7

Keywords

Fetal alcohol syndrome; Eyeblink conditioning; Arithmetic; Fetal alcohol spectrum disorders; Biomarkers; Behavioral phenotype; Prenatal alcohol exposure

Funding

  1. NIH/National Institute on Alcohol Abuse and Alcoholism (NIAAA) [R01 AA06966, R01 AA09524, and P50 AA0706]
  2. NIH Office of Research on Minority Health [R01-AA09524]
  3. Foundation for Alcohol Related Research, Cape Town, South Africa
  4. NIAAA Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD) [U01 AA014790]
  5. NIH [R03 TW007030]
  6. Office of the President of Wayne State University [FA2005040800024]
  7. National Research Foundation of South Africa
  8. South African Research Chairs Initiative of the Department of Science and Technology and National Research Foundation of South Africa
  9. University of Cape Town
  10. CIFASD [U24 AA014815]
  11. State of Michigan

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Identification of children with fetal alcohol spectrum disorders (FASD) is difficult because information regarding prenatal exposure is often lacking, a large proportion of affected children do not exhibit facial anomalies, and no distinctive behavioral phenotype has been identified. Castellanos and Tannock have advocated going beyond descriptive symptom-based approaches to diagnosis to identify biomarkers derived from cognitive neuroscience. Classical eyeblink conditioning and magnitude comparison are particularly promising biobehavioral markers of FASD-eyeblink conditioning because a deficit in this elemental form of learning characterizes a very large proportion of alcohol-exposed children; magnitude comparison because it is a domain of higher order cognitive function that is among the most sensitive to fetal alcohol exposure. Because the neural circuitry mediating both these biobehavioral markers is well understood, they have considerable potential for advancing understanding of the pathophysiology of FASD, which can contribute to development of treatments targeted to the specific deficits that characterize this disorder.

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