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The Center for Education and Drug Abuse Research

School of Pharmacy

University of Pittsburgh

Center for Education and Drug Abuse Research

CEDAR Research Modules Components

Neurocognition (Coordinator: Ralph Tarter, Ph.D.)

  1. Document the relative influence of executive cognitive function (ECF) capacity and general neurocognitive ability in childhood (ages 10-12) on substance involvement in adolescence (age 16) and transition to a diagnosis of substance use disorders (SUD).
  2. Determine the relation between family environment adversity and executive cognitive functioning (ECF and non-specific cognitive capacity.
  3. Examine the role of ECF and non-ECF general cognitive capacity in the intergenerational transmission of SUD liability.
  4. Elucidate the extent to which synchrony between ECF capacity and sexual maturation predicts age of onset of substance use, rate of change in substance use behavior over time, and age of first SUD diagnosis.
  5. Elucidate the association between ECF and the P300 component of the event related potential (ERP) on the risk for SUD
Developmental/Psychopathology (Coordinator: Duncan Clark, Ph.D., M.D.)

  1. Characterize the development of psychopathological characteristics in relation to SUD liability from late childhood through young adulthood, emphasizing the differential influences of gender and patterns of psychopathology among family members
  2. Determine prospectively the impact of psychopathology in childhood and adolescence on drug use initiation and its acceleration leading to SUD.
  3. Determine the extent to which behavioral and affective dysregulation covary with and predict substance topology and SUD onset age and severity
Genetics ModuleĀ  (Coordinator: Michael Vanyukov, Ph.D)

  1. Evaluate the associations of SUD liability with individual DNA polymorphisms and haplotypes at the loci involved in neurochemical systems critical in drug-related reinforcement (e.g. dopaminergic, serotonergic, opiodergic, etc.), using population-based and family-based paradigms controlling for population stratification in conjunction with measured haplotype analysis (MHA) and complementary statistical methods.
  2. Within the loci associated with SUD liability, identify polymorphisms affecting SUD risk; test their influence using peripheral indicators of gene function.
  3. Estimate the effect of interactions between the candidate genes on SUD liability.
  4. Demonstrate that the genetic and environmental contribution to variation in the risk for SUD is mediated by behavior and affect dysregulation during childhood.
Family and Social Ecology Module (Coordinator: Ada Mezzich, Ph.D.)

  1. Determine the extent to which there is a reciprocal influence of risk and protective family relationships and parenting practices among parent-index and sibship dyads at at ages 10-12-, 12-14 and 16 predicting index's substance use severity (SUS) score at age 19.
  2. Determine the family, peer and neighborhood factors, including exposure to stressors, that moderate the relationship between neurobehavior disinhibition (ND) and level of substance use involvement across four timepoints of assessment (ages 10-12, 12-14, 16 and 19).
  3. Delineate the factors in the environment (family, peers, neighborhood), in conjunction with ND phenotype, genotype and stressors, that borth directly contribute to and moderate the association between substance use and SUD across ages 10-12, 12-14, 16 and 19.
  4. Determine the role of quality of family, peer, and neighborhood environments in the cross-generational transmissibility of substance use involvement.