A Concentration Killer: Study Shows Brain Chemistry Defect Is Key To Attention,,Deficit Hyperactivity Disorder In Adults

WASHINGTON, D.C. August 3 -- For the first time, research directly points to a dopamine production defect in adults with attention deficit hyperactivity disorder (ADHD). The brain chemical findings could lead to more effective treatments for these patients who are inattentive, impulsive, and hyperactive.

Previous evidence suggested that a dopamine malfunction occurs in those with ADHD. For example, drugs that enhance dopamine function appear to quell the disorder's symptoms. "Our finding, however, is the first direct evidence of a targeted dopamine deficit in adults with ADHD," says the study's lead author, Monique Ernst, MD, PhD, Senior Staff Fellow at the National Institutes of Health. "We found that the activity of an enzyme involved in the production of the chemical dopamine is lower than normal in a specific brain area."

Ernst's study, funded by the National Institutes of Health, is published in the August 1 issue of The Journal of Neuroscience.

ADHD is estimated to affect three percent to five percent of American school-aged children, perhaps as many as 3.5 million youngsters, according to the National Institute of Mental Health. Up to 60 percent of these children will continue to experience symptoms in adulthood.

"Ernst's study is an exciting and potentially very significant finding regarding the neural basis of ADHD and its developmental progression," says ADHD expert B.J. Casey, PhD, of the University of Pittsburgh Medical Center.

In the study, the researchers analyzed the brains of 17 ADHD adults with positron emission tomography (PET). The PET images, which highlighted the activity of the dopamine-producing enzyme, DOPA decarboxylase, indicate that an abnormality in dopamine production occurs in only one of the dopamine-rich brain regions, the anterior frontal cortex. This region underlies motor activity and cognitive processes, including attention. "A better understanding of the deficit

Contact: Leah Ariniello
Society for Neuroscience

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