FAMILY STUDY OF NEUROPSYCHOLOGICAL RISK FOR ALCOHOLISM

申请人摘要：神经心理学风险标志物 执行和抑制过程，沿着先前的行为风险， 注意力缺陷多动障碍（ADHD）和行为问题的形式， 两者都被确定为酗酒/问题的预测因子，尽管 这些风险结构相互作用的方式 酒精问题的终点仍然不确定。两项相互关联的研究旨在 澄清这个问题。研究I是一项家庭研究，探讨额叶皮层在脑梗死中的作用。 神经心理学机制作为发展中的潜在介质 已知青少年中的酒精问题有较高的风险， 结果。执行功能的三部分模型指导 神经心理学评估酗酒风险增加的特点是家庭 历史，但假设是通过额叶神经认知的方式传达 损伤在一个密集的社会化结构中长大， 鼓励后来的酒精相关的困难也假设， 调解这种关系。儿童行为风险（ADHD或行为问题）是 假设调解神经心理风险和 以及家族史，来预测酒精问题的结果。 这些假设将在一项正在进行的前瞻性研究中进行检验， 酗酒者及其父母的男性和女性子女（n=214个家庭）， 沿着的还有一组生态上相当但不含酒精的对照组 家庭（n=79）。每隔3年进行一次评估， 参与者目前正在进入酒精可能发作期 使用和酒精问题（即，12-14岁）。神经心理学协议 当儿童参与者年龄为12-14岁且父母平均年龄为 年龄39岁（S.D.= 5.7）。 发育进展将通过平行评估 对15-17岁和18-20岁的青年进行评估。 正在进行的纵向研究设计，涉及父母以及 儿童，允许同时进行研究II，研究稳定性 成年酗酒者额叶神经认知功能障碍的变化 成年中期，研究这种损害与这些 成年受试者持续的心理社会和酒精适应。还要 研究的是神经心理缺陷作为一种潜在的 父母作为有效社交者的能力的中介， 后代父母反社会共病水平的实质性变化， 以及缓解状态，将使这两项研究能够解决以下问题： 结果的异质性在两个COA和酗酒的成年人。

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.