12-months of treatment with ADHD drugs increases dopamine transporters in some brain regions by 24%

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Long-term ADHD treatment increases brain dopamine transporter levels, may affect drug efficacy

12-month treatment may impact adult ADHD patients’ response to methylphenidate

Long-term treatment of attention deficit/hyperactivity disorder (ADHD) with certain stimulant medications may alter the density of the dopamine transporter, according to research published May 15 in the open access journal PLOS ONE by Gene-Jack Wang and colleagues from Brookhaven National Laboratory and the intramural program at NIH.

ADHD is commonly treated using drugs to target dysfunctional dopamine signaling in the brain, such as methylphenidate (commonly known as Ritalin). The researchers found that adults with ADHD who had been prescribed the drug methylphenidate for a period of 12 months had a 24% increase in the density of the dopamine transporter in some brain regions, which after treatment was significantly higher than in adults without ADHD who had not been treated with the drug. Prior to the 12-month treatment, there were no significant differences in the two groups’ dopamine transporter levels. The authors conclude that the elevated dopamine transporter density, suggested by some as a biological test for diagnosis of ADHD, may be a consequence of chronic treatment rather than a marker for the disorder. These findings may offer an explanation for discrepancies in the literature describing dopamine transporter levels in ADHD patients, as differences in dopamine transporter levels in the brain may be due to differences in prior treatment.

Many studies have shown that an acute increase in dopamine signaling while on methylphenidate treatment can improve ADHD symptoms in the short term, but this is the first study to analyze the long-term effects of treatment.


Citation: Wang G-J, Volkow ND, Wigal T, Kollins SH, Newcorn JH, et al. (2013) Long-Term Stimulant Treatment Affects Brain Dopamine Transporter Level in Patients with Attention Deficit Hyperactive Disorder. PLoS ONE 8(5): e63023. doi:10.1371/journal.pone.0063023

Financial Disclosure: The work was supported by the National Institutes of Health: R01MH66961 to Dr. GJW. The PET study was carried out at Brookhaven National Laboratory with infrastructure support from the U.S. Department of Energy Office of Biological and Environmental Research (DE-ACO2-76CH00016), M01RR10710 (the General Clinical Research Center of Stony Brook University). An Intramural Research Program of the National Institute on Alcohol Abuse and Alcoholism (Z01AA000550) supported Drs. NDV and FT and Mr. MJ. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interest Statement: Dr. GJW received research funding from the Orexigen Therapeutics Inc.; Dr. NDV reports no competing interests; Dr. TW reports no competing interests; Dr. SHK reports no competing interests; Dr. JHN reports no competing interests; Dr. FT reports no competing interests; Dr. JL reports no competing interests; Mr. MJ reports no competing interests; Mr. CTW reports no competing interests; Mr. HH reports no competing interests; Dr. JSF reports no competing interests; Dr. WZ reports no competing interests; Dr. JMS reports no competing interests. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials.

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