4.5 Article

New potential leads in the biology and treatment of attention deficit-hyperactivity disorder

Journal

CURRENT OPINION IN NEUROLOGY
Volume 20, Issue 2, Pages 119-124

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WCO.0b013e3280a02f78

Keywords

attention deficit-hyperactivity disorder; dopamine; genetics; neuroimaging; prefrontal cortex

Funding

  1. NATIONAL INSTITUTE OF MENTAL HEALTH [R21MH070542, R01MH064166] Funding Source: NIH RePORTER
  2. NATIONAL INSTITUTE ON DRUG ABUSE [R01DA018879] Funding Source: NIH RePORTER
  3. NIDA NIH HHS [R01 DA018879] Funding Source: Medline
  4. NIMH NIH HHS [R01 MH064166, R21 MH 070542] Funding Source: Medline

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Purpose of review This review highlights recent neuroimaging and genetic studies of attention deficit-hyperactivity disorder that may inform biologically targeted interventions and treatments. Recent findings The findings suggest that attention deficit-hyperactivity disorder is characterized by specific learning and cognitive deficits due to abnormalities in dopamine-rich prefrontal circuitry, of genetic or environmental origins. In addition to prefrontal cortical areas, the basal ganglia, cerebellum, and parietal cortex have been implicated in the condition. These regions are part of unique circuits that project both to and from the prefrontal cortex, thus providing a means for signaling prefrontal regions when top-down control of behavior needs to be imposed. Ineffective signaling of control systems by any one of these regions can lead to poor regulation of behavior. Likewise, intact signaling but inefficient top-down control could result in poor regulation of behavior. Summary Identification of which cognitive and neural processes are altered in attention deficit-hyperactivity disorder and acknowledgement of different casuses of the condition will lead to more individualized, biologically targeted interventions and treatments. This new direction in research and treatment has occurred as the result of a shift from diagnosis as a phenotype, to refined phenotypes of core cognitive deficits that can be more easily tied to the underlying biology.

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