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Neurogenetic interactions and aberrant behavioral co-morbidity of attention deficit hyperactivity disorder (ADHD): dispelling myths

David E Comings1 email, Thomas JH Chen2 email, Kenneth Blum3 email, Julie F Mengucci4 email, Seth H Blum4 email and Brian Meshkin5 email

1Director, Carlsbad Science Foundation, Emeritus Professor City of Hope Medical Center, Duarte, California, USA

2Changhua Christian Hospital, Taiwan, Republic Of China

3Wake Forest University School Of Medicine, Department Physiology & Pharmacology, Medical Center Boulevard, Winston -Salem, North Carolina, Salugen, Inc. San Diego, California, USA

4Synapatmine, Inc., San Antonio, Texas, USA

5Salugen, Inc., San Diego, California, USA

author email corresponding author email

Theoretical Biology and Medical Modelling 2005, 2:50doi:10.1186/1742-4682-2-50

Published: 23 December 2005

Abstract

Background

Attention Deficit Hyperactivity Disorder, commonly referred to as ADHD, is a common, complex, predominately genetic but highly treatable disorder, which in its more severe form has such a profound effect on brain function that every aspect of the life of an affected individual may be permanently compromised. Despite the broad base of scientific investigation over the past 50 years supporting this statement, there are still many misconceptions about ADHD. These include believing the disorder does not exist, that all children have symptoms of ADHD, that if it does exist it is grossly over-diagnosed and over-treated, and that the treatment is dangerous and leads to a propensity to drug addiction. Since most misconceptions contain elements of truth, where does the reality lie?

Results

We have reviewed the literature to evaluate some of the claims and counter-claims. The evidence suggests that ADHD is primarily a polygenic disorder involving at least 50 genes, including those encoding enzymes of neurotransmitter metabolism, neurotransmitter transporters and receptors. Because of its polygenic nature, ADHD is often accompanied by other behavioral abnormalities. It is present in adults as well as children, but in itself it does not necessarily impair function in adult life; associated disorders, however, may do so. A range of treatment options is reviewed and the mechanisms responsible for the efficacy of standard drug treatments are considered.

Conclusion

The genes so far implicated in ADHD account for only part of the total picture. Identification of the remaining genes and characterization of their interactions is likely to establish ADHD firmly as a biological disorder and to lead to better methods of diagnosis and treatment.


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