This request for a renewal of funding is in response to the NIH/NIAAA funding opportunity entitled, "Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD)" (RFA-AA-12-004). The proposed study is relevant to the overall goal of the CIFASD funding opportunity of "further refining definitive diagnoses of FASD at different stages of the lifespan based on biological, physical, neurological, or behavioral assessment, or a combination thereof." It is also directly in line with three of the specific research areas identifed in the RFA: (1) Enhanced understanding of the neurobehavioral phenotype of FAS and ARND, (2) Diagnosis of FASD, and (3) Early case identification. Although nearly 40 years have passed since the initial clinical delineation of fetal alcohol syndrome (FAS), understanding of the full spectrum of effects of prenatal alcohol exposure (AE) is incomplete. Even though many children with AE experience significant neurobehavioral and adaptive difficulties that are related to their exposure history, for a majority of the cases, the link between those difficulties and AE may go unrecognized. Given that early identification has been linked to improved prognosis, it is critical to improve identification of alcohol-affected children with a sensitive, clinically utilizable neurobehavioral profile. Recent research, including that funded by CIFASD, has focused on the specificity of alcohol's effects by comparing children with AE and those with attention-deficit/hyperactivity disorder (ADHD). While this research has documented important similarities and differences between AE and ADHD, comparisons with a more heterogeneous contrast group may increase the generalizability of the profile as well as detect deficits that are common between neurodevelopmental conditions and those that are unique to the effects of prenatal alcohol exposure. Finally, previous work on the neurobehavioral profile has focused primarily on the executive function domain, however, preliminary data and previous research suggests that including measures of memory function may strengthen the existing profile. The overarching aim of the current proposal is to develop and implement clinically relevant and feasible measurement tools to accurately identify children who are affected by AE. The proposed study will build on our existing database derived from data collected from children between 8-16 years of age, across multiple clinical sites and expand it to include two age groups (5-7 years and 10-16 years) to improve early identification, as well as assess an additional neuropsychological domain (memory). Data will be collected from children with AE, non-exposed controls and heterogeneous clinical contrast subjects at both new and existing sites. This research will improve understanding of fetal alcohol spectrum disorders (FASD) by continuing ongoing efforts to develop and refine a sensitive and specific neurobehavioral profile. These data will be combined with data from other CIFASD projects to develop models that accurately capture the greatest number of affected children using multidisciplinary methodology.

Public Health Relevance

This project is directly relevant to public health concerns surrounding the effects of heavy prenatal alcohol exposure, defining the profile of neurobehavioral effects that are specific to alcohol, and improving identification of alcohol-affected individuals at younger ages. Improved identification and delineation of these features, especially in younger children, will ultimately lead to improved treatment.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Research Project--Cooperative Agreements (U01)
Project #
5U01AA014834-10
Application #
8527619
Study Section
Special Emphasis Panel (ZAA1-CC (02))
Program Officer
Dunty, Jr, William
Project Start
2003-09-30
Project End
2017-05-31
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
10
Fiscal Year
2013
Total Cost
$548,566
Indirect Cost
$84,398
Name
San Diego State University
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
073371346
City
San Diego
State
CA
Country
United States
Zip Code
92182
Panczakiewicz, Amy L; Glass, Leila; Coles, Claire D et al. (2016) Neurobehavioral Deficits Consistent Across Age and Sex in Youth with Prenatal Alcohol Exposure. Alcohol Clin Exp Res 40:1971-81
Graham, Diana M; Glass, Leila; Mattson, Sarah N (2016) The Influence of Extrinsic Reinforcement on Children with Heavy Prenatal Alcohol Exposure. Alcohol Clin Exp Res 40:348-58
Wozniak, Jeffrey R; Mueller, Bryon A; Mattson, Sarah N et al. (2016) Functional connectivity abnormalities and associated cognitive deficits in fetal alcohol Spectrum disorders (FASD). Brain Imaging Behav :
Goh, Patrick K; Doyle, Lauren R; Glass, Leila et al. (2016) A Decision Tree to Identify Children Affected by Prenatal Alcohol Exposure. J Pediatr 177:121-127.e1
Moore, Eileen M; Infante, M Alejandra; Migliorini, Robyn et al. (2016) Pituitary lacks sexual dimorphism and displays reduced signal intensity on T1-weighted MRI in adolescents with histories of heavy prenatal alcohol exposure. Neurotoxicol Teratol 57:106-111
Gautam, P; Nuñez, S C; Narr, K L et al. (2015) Developmental Trajectories for Visuo-Spatial Attention are Altered by Prenatal Alcohol Exposure: A Longitudinal FMRI Study. Cereb Cortex 25:4761-71
Doyle, Lauren R; Mattson, Sarah N (2015) Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): Review of Evidence and Guidelines for Assessment. Curr Dev Disord Rep 2:175-186
Gautam, Prapti; Lebel, Catherine; Narr, Katherine L et al. (2015) Volume changes and brain-behavior relationships in white matter and subcortical gray matter in children with prenatal alcohol exposure. Hum Brain Mapp 36:2318-29
Nguyen, Tanya T; Glass, Leila; Coles, Claire D et al. (2014) The clinical utility and specificity of parent report of executive function among children with prenatal alcohol exposure. J Int Neuropsychol Soc 20:704-16
Glass, Leila; Graham, Diana M; Deweese, Benjamin N et al. (2014) Correspondence of parent report and laboratory measures of inattention and hyperactivity in children with heavy prenatal alcohol exposure. Neurotoxicol Teratol 42:43-50

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