UCLA

Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset disorder characterized by developmentally-aberrant and impairing levels of inattention and/or hyperactivity-impulsivity (Diagnostic and Statistical Manual of Mental Disorders, 4th edition - Text Revision; American Psychiatric Association, 2000). ADHD affects approximately 8-12% of school-aged children worldwide (Froehlich et al., 2007), and prospectively predicts a wide range of negative outcomes, including academic failure, criminality, substance abuse, and neuropsychological impairment (Barkley & Fischer, 2010; Langley et al., 2010; Molina et al., 2009).

Although there is consensus that ADHD is influenced by biological (e.g., genetics) and environmental factors (e.g., parenting) (Nigg, Nikolas, & Burt, 2010; Plomin, Owen, & McGuffin, 1994), relatively little research has directly assessed how biological and environmental factors interact in the development of ADHD and other forms of psychopathology (Moffitt, Caspi, & Rutter, 2006). Genetic influences on psychopathology are likely to depend on exposure to or the experience of varying environmental conditions such that some children exposed to environmental adversity (e.g., abuse, maladaptive parenting) develop psychopathology whereas others do not (i.e., gene x environment interaction; G×E ) (Waldman, 2007). The primary aim of this study is to investigate the interactive effects of several functional polymorphisms and their interaction with environmental factors that are known to influence ADHD and related phenotypes. My dissertation will interrogate these influences using multiple research designs (i.e., cross-sectional, longitudinal) and methods (i.e., rating scales, experimental manipulations), including a large prospective longitudinal study of unselected youth and an intensively characterized sample of school-age children with and without ADHD being followed prospectively.