Attention-deficit/hyperactivity disorder (adhd) as a noradrenergic disorder

  title={Attention-deficit/hyperactivity disorder (adhd) as a noradrenergic disorder},
  author={Joseph Biederman and Thomas J. Spencer},
  journal={Biological Psychiatry},

Novel approach to evaluate central autonomic regulation in attention deficit/hyperactivity disorder (ADHD).

Evaluation of central autonomic regulation by noninvasive methods, namely pupillometry and eye-tracking, may provide novel information for better understanding of the neurobiological pathomechanisms leading to ADHD.

Catecholamine Dysfunction in Attention-Deficit/Hyperactivity Disorder: An Update

  • J. Prince
  • Psychology, Biology
    Journal of clinical psychopharmacology
  • 2008
This article focuses on the catecholaminergic networks of higher cognitive functions such as attention and focus and of motor functions that may be associated with such networks, reviewing both the physiology of such functions and the pathophysiology of ADHD.

Linkage study of the alpha2A adrenergic receptor in attention-deficit hyperactivity disorder families.

The possibility that the gene for the alpha2A adrenergic receptor (ADRA2A) is linked to ADHD is examined by testing a polymorphism located in the promoter region of the ADRA2A gene in a sample of 94 nuclear families with an ADHD proband and found no evidence for linkage.

Linkage studies between attention-deficit hyperactivity disorder and the monoamine oxidase genes.

Testing for linkage between ADHD and the MAOA gene and DSM-III-R-diagnosed ADHD in 82 nuclear families of the Chinese population suggested that MAOA might be a susceptibility factor for ADHD.

Pharmacotherapy for Attention-Deficit/Hyperactivity Disorder: From Cells to Circuits

The present review outlines the actions of ADHD medications from subcellular effects to effects on neural systems and cognition in ADHD patients and outlines the very active area of investigation at all phases of the translational cycle.

The norepinephrine transporter gene and attention-deficit hyperactivity disorder.

The results do not support the NET1 gene as a major genetic susceptibility factor in ADHD.

No Evidence of an Association between Norepinephrine Transporter Gene Polymorphisms and Attention Deficit Hyperactivity Disorder

The findings do not support SLC6A2 as a major genetic susceptibility factor in ADHD.

Executive dysfunction in attention-deficit/hyperactivity disorder: cognitive and neuroimaging findings.

  • R. RothA. Saykin
  • Psychology, Biology
    The Psychiatric clinics of North America
  • 2004



Neurobiology of attention-deficit hyperactivity disorder

Association of attention-deficit disorder and the dopamine transporter gene.

Attention-deficit hyperactivity disorder (ADHD) has been shown to be familial and heritable, in previous studies. As with most psychiatric disorders, examination of pedigrees has not revealed a

Catecholamines in attention-deficit hyperactivity disorder: current perspectives.

A multistage hypothesis is presented which emphasizes the interaction of norepinephrine, epinephrine, and dopamine in modulation of attention and impulse control.

Confirmation of association between attention deficit hyperactivity disorder and a dopamine transporter polymorphism

A 3′ variable number of tandem repeat (VNTR) polymorphism at the dopamine transporter gene (DAT1) in a sample of 49 ADHD patients and their parents is examined using the haplotype relative risk (HRR) method, finding that the 480-bp allele was preferentially transmitted to ADHD probands.

Association and linkage of the dopamine transporter gene and attention-deficit hyperactivity disorder in children: heterogeneity owing to diagnostic subtype and severity.

The results replicate and extend previous findings of the association between the DAT1 gene and childhood ADHD and represent one of the first replicated relations of a candidate gene and a psychiatric disorder in children.

Dopamine D4 gene 7-repeat allele and attention deficit hyperactivity disorder.

OBJECTIVE Family, twin, and adoption studies show attention deficit hyperactivity disorder (ADHD) to have a substantial genetic component, and some studies have reported an association between ADHD

Dopamine D4 receptor gene polymorphism is associated with attention deficit hyperactivity disorder.

The present findings suggest that polymorphic variation in the gene encoding the D4 dopamine receptor may be a contributing factor in the expression of symptoms associated with ADHD.

Is Attention Deficit Hyperactivity Disorder Familial?

Although the available literature provides strong evidence for the familial transmission of attention deficit hyperactivity disorder, the mode of transmission requires further clarification, and attention deficithyperactivity disorder appears to be genetically heterogeneous, indicating that more work is needed to delineate genetically homogeneous subtypes and to describe the range of expression of their underlying genotypes.

Desipramine treatment of children with attention-deficit hyperactivity disorder and tic disorder or Tourette's syndrome.

The magnitude and persistence of the response is encouraging and suggest a therapeutic role for DMI in the treatment of CTD + ADHD patients, which can be seen as preliminary only until replicated in a controlled investigation.