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PubMed · 14694701

Attention-deficit hyperactivity disorder.

Ajay K Thapar·Anita Thapar
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Abstract

Attention-deficit hyperactivity disorder (ADHD) affects between 1.4% and 6% of children. The importance of the role of primary care in the recognition and joint management of this disorder is being increasingly highlighted. Despite a wealth of research, the diagnosis and management of ADHD have attracted a good deal of controversy. In this discussion paper, we focus on the empirical basis for some of the more controversial aspects of ADHD, such as diagnosis (discussing both under- and overdiagnosis), aetiology, outcomes, and the role of psychosocial factors in this disorder. We conclude that, provided the diagnosis of ADHD is made accurately and systematically, there are no good scientific grounds for dismissing the concept of ADHD or for failing to intervene.

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Attention Deficit Disorder with HyperactivityFamily PracticeHumansPhysician's RolePractice Patterns, Physicians'PrognosisReferral and ConsultationJournal ArticleReview

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BibTeXRIS

Ajay K Thapar, Anita Thapar. 2003. Attention-deficit hyperactivity disorder.. https://pubmed.ncbi.nlm.nih.gov/14694701/

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PubMed2005

Identification and characterization of human NR4A2 polymorphisms in attention deficit hyperactivity disorder.

Attention deficit hyperactivity disorder (ADHD) is a highly heritable and common disorder thought to arise, in part, from alterations in dopamine function. NR4A2, or Nurr1, is an orphan nuclear receptor implicated in the development of dopaminergic cells of the ventral tegmental area (VTA) and the substantia nigra (SN). Dopaminergic cells of the VTA provide innervation to the prefrontal cortex, believed to be of major importance in the etiology of ADHD, suggesting that NR4A2 is a potential candidate gene for ADHD susceptibility. This study aimed to identify polymorphisms in NR4A2 and test their association to ADHD. Database analysis revealed a CA repeat polymorphism in the 3' UTR of NR4A2 that was confirmed by PCR. SSCP screening revealed a common DeltaC polymorphism, 254 bp 5' to the transcriptional start site. These polymorphisms were tested for an association with ADHD in both a case control study of individuals from the Milwaukee Longitudinal Study of ADHD (103 cases and 66 controls), and in 35 families composed of trios or affected sib pairs (ASP) with ADHD. Functional effects of the promoter polymorphism were tested in vitro. The non-deleted allele was significantly more active in undifferentiated SK-N-MC cells compared to differentiated SK-N-MC and HeLa cells while a trend for increased activity for the DeltaC allele was observed in undifferentiated SK-N-MC cells. Identification of these polymorphisms may aid future candidate gene studies in disorders with altered dopamine signaling, such as schizophrenia Parkinson's disease and ADHD.

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