FAMILY STUDY OF NEUROPSYCHOLOGICAL RISK FOR ALCOHOLISM

点击翻译按钮获取中文摘要

APPLICANT'S ABSTRACT: Neuropsychological markers of risk pertaining to executive and inhibitory processes, along with prior behavioral risk in the form of attention deficit-hyperactivity disorder (ADHD) and conduct problems, have both been established as predictors of alcohol abuse/problems, although the manner in which these risk structures interact in contributing to the alcohol problem endpoint remains uncertain. Two inter-related studies aim to elucidate this issue. Study I is a family study of the role of frontal neuropsychological mechanisms as potential mediators in the development of alcohol problems among adolescents known to be at elevated risk for such outcomes. A three part model of executive function guides the neuropsychological assessment. Increased alcoholism risk is marked by family history, but is hypothesized to be conveyed by way of frontal neurocognitive impairment. Rearing in a socialization structure that is dense for the encouragement of later alcohol related difficulty is also hypothesized to mediate this relationship. Child behavioral risk (ADHD or conduct problems) is hypothesized to mediate the relationship of both neuropsychological risk as well as family history, in predicting an alcohol problem outcome. These hypotheses are to be tested in an already ongoing prospective study of male and female children of alcoholics and their parents (n=214 families), along with an ecologically comparable but nonalcoholic group of control families (n=79 families). Assessments occur at 3 year intervals, and the child participants are currently entering the period of probable onset for alcohol use and alcohol problems (i.e., ages 12-14). The neuropsychological protocol is to be added when child participants are age 12-14 and parents are at mean age 39(S.D.=5.7). Developmental progression is to be evaluated by parallel assessments when youth are ages 15-17 and 18-20. The ongoing Longitudinal Study design, involving parents as well as the children, allows the simultaneous conduct of Study II, a study of stability and change in frontal neurocognitive impairment among adult alcoholics in middle adulthood, that examines the relationship of such impairment to these adult subjects' ongoing psychosocial and alcoholic adaptation. Also to be examined is the role of the neuropsychological deficits as a potential mediator of parents' ability to act as effective socializers for their offspring. Substantial variations in level of parental antisocial comorbidity, as well as remission status, will allow both studies to address issues of heterogeneity of outcome among both the COAs and the alcoholic adults.