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The immune system may be involved in the susceptibility to childhood attention deficit hyperactivity disorder (ADHD)

Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder, characterized by inattention, hyperactivity and impulsivity. It affects 4- 10% of school age children, exacting a significant clinical and public health toll. ADHD constitutes one of the main reasons for referral to neurological/psychiatric treatment in this age group, and results in exposure of many children to prolonged courses of stimulant medication such as Ritalin. Untreated, ADHD may lead to impairments in schooling and social adaptation in a critical period of development, eventuating in damage to the childs self esteem and personality development, with high rates of depression, conduct disorder, school dropouts, and substance abuse. The causes of ADHD are unknown. Current theories suggest altered brain activity of chemical transmitters such as dopamine and norepinepherine may play a role. This is based on pharmacological observations showing reduction in symptoms in response to stimulant drugs such as Ritalin which augment dopaminergic and noradrenergic activity in relevant brain areas. However, current findings evade simplistic neurochemical explanations.

Family studies suggest a major heritable contribution to ADHD, but the mode of inheritance remains obscure. To date, the search for actual genes involved focused mainly on the dopamine system, with some findings suggesting a possible involvement of dopaminergic genes in risk for ADHD.

The current study, is the first to report the possible involvement of a gene encoding a modulator of the immune system in ADHD. Recent evidence supports the involvement of immune modulators in brain processes outside the realm of their classical role in inflammatory responses. One of the major modulators, interleukin 1 (IL-1) is expressed in the adult brain, and plays a role in maintaining neural plasticity, neuroprotection, and response to non immune stressors. Recent theories suggest it may be involved in ps
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Contact: Karl Lorenzen
molecularpsychiatry@mednet.ucla.edu
310-206-6739
Molecular Psychiatry
7-Jan-2002


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