Attention-deficit hyperactivity disorder (ADHD) is the most commonly diagnosed psychiatric disorder of childhood. ADHD is characterized by inattention, hyperactivity, distractibility, nd other disruptive behaviors. Studies show that ADHD persists into adulthood in 10%-60% of childhood-onset cases with many dults showing high levels of comorbidity. In the majority of ADHD cases, no etiology has been determined. Discussions and research on the leading causes of ADHD focus on genetic factors, perinatal factors, infections and neurobiologic events. Studies over the past 30 years indicate that genetics is of etiological importance in this illness. Recent neurobiological findings and results from assoication studies suggest that genes associated with catecholamine mechanisms or neurodevelopmental processes may be involved in the etiology of ADHD. The herogeneity of ADHD suggests an etiology which could involve several different mutations at several loci or, alternatively, several genes could act together with each having a small effect. Given these parameters, it may be more dvantageous to rely on large samples of smaller, homogenous families rather than a heterogenous group of families or large pedigrees, both of which could obscure genetic mechanisms. This study will explore the genetic and molecular mechanisms involved in ADHD.
the specific aims i nclude: (1) case identification of probands with ADHD; (2) careful differential diagnosis after initial presentation with proper identification of comorbid conditions; (3) collectioin of a large sample of nuclear families who are well characterized ans subtyped by fmily history and phenotype definitions; (4) application of molecular genetic techniques to examine loci involved in catecholamine mechanisms and neuro- developmental processes related to attention systems.
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