The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD): What every clinician should know

Samuele Cortese

Research output: Contribution to journalArticle

112 Citations (Scopus)

Abstract

This review, addressed mainly to clinicians, considers commonly asked questions related to the neuroimaging, neurophysiology, neurochemistry and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD). It provides answers based on the most recent meta-analyses and systematic reviews, as well as additional relevant original studies. Empirical findings from neurobiological research into ADHD reflect a shift in the conceptualisation of this disorder from simple theoretical views of a few isolated dysfunctions to more complex models integrating the heterogeneity of the clinical manifestations of ADHD. Thus, findings from structural and functional neuroimaging suggest the involvement of developmentally abnormal brain networks related to cognition, attention, emotion and sensorimotor functions. Brain functioning alterations are confirmed by neurophysiological findings, showing that individuals with ADHD have elevated theta/beta power ratios, and less pronounced responses and longer latencies of event-related potentials, compared with controls. At a molecular level, alterations in any single neurotransmitter system are unlikely to explain the complexity of ADHD; rather, the disorder has been linked to dysfunctions in several systems, including the dopaminergic, adrenergic, serotoninergic and cholinergic pathways. Genetic studies showing a heritability of ∼60-75% suggest that a plethora of genes, each one with a small but significant effect, interact with environmental factors to increase the susceptibility to ADHD. Currently, findings from neurobiological research do not have a direct application in daily clinical practice, but it is hoped that in the near future they will complement the diagnostic process and contribute to the long-term effective treatment of this impairing condition.

Original languageEnglish
Pages (from-to)422-433
Number of pages12
JournalEuropean Journal of Paediatric Neurology
Volume16
Issue number5
DOIs
Publication statusPublished - Sep 2012

Fingerprint

Neurobiology
Attention Deficit Disorder with Hyperactivity
Neurochemistry
Neurophysiology
Functional Neuroimaging
Brain
Evoked Potentials
Research
Neuroimaging
Adrenergic Agents
Cognition
Cholinergic Agents
Reaction Time
Neurotransmitter Agents
Meta-Analysis
Emotions
Genes

Keywords

  • ADHD
  • Genetics
  • Neurobiology
  • Neurochemistry
  • Neuroimaging
  • Neurophysiology

ASJC Scopus subject areas

  • Clinical Neurology
  • Pediatrics, Perinatology, and Child Health

Cite this

The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD) : What every clinician should know. / Cortese, Samuele.

In: European Journal of Paediatric Neurology, Vol. 16, No. 5, 09.2012, p. 422-433.

Research output: Contribution to journalArticle

@article{5d4b753e97f64629a883182c59020eb3,
title = "The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD): What every clinician should know",
abstract = "This review, addressed mainly to clinicians, considers commonly asked questions related to the neuroimaging, neurophysiology, neurochemistry and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD). It provides answers based on the most recent meta-analyses and systematic reviews, as well as additional relevant original studies. Empirical findings from neurobiological research into ADHD reflect a shift in the conceptualisation of this disorder from simple theoretical views of a few isolated dysfunctions to more complex models integrating the heterogeneity of the clinical manifestations of ADHD. Thus, findings from structural and functional neuroimaging suggest the involvement of developmentally abnormal brain networks related to cognition, attention, emotion and sensorimotor functions. Brain functioning alterations are confirmed by neurophysiological findings, showing that individuals with ADHD have elevated theta/beta power ratios, and less pronounced responses and longer latencies of event-related potentials, compared with controls. At a molecular level, alterations in any single neurotransmitter system are unlikely to explain the complexity of ADHD; rather, the disorder has been linked to dysfunctions in several systems, including the dopaminergic, adrenergic, serotoninergic and cholinergic pathways. Genetic studies showing a heritability of ∼60-75{\%} suggest that a plethora of genes, each one with a small but significant effect, interact with environmental factors to increase the susceptibility to ADHD. Currently, findings from neurobiological research do not have a direct application in daily clinical practice, but it is hoped that in the near future they will complement the diagnostic process and contribute to the long-term effective treatment of this impairing condition.",
keywords = "ADHD, Genetics, Neurobiology, Neurochemistry, Neuroimaging, Neurophysiology",
author = "Samuele Cortese",
year = "2012",
month = "9",
doi = "10.1016/j.ejpn.2012.01.009",
language = "English",
volume = "16",
pages = "422--433",
journal = "European Journal of Paediatric Neurology",
issn = "1090-3798",
publisher = "W.B. Saunders Ltd",
number = "5",

}

TY - JOUR

T1 - The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD)

T2 - What every clinician should know

AU - Cortese, Samuele

PY - 2012/9

Y1 - 2012/9

N2 - This review, addressed mainly to clinicians, considers commonly asked questions related to the neuroimaging, neurophysiology, neurochemistry and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD). It provides answers based on the most recent meta-analyses and systematic reviews, as well as additional relevant original studies. Empirical findings from neurobiological research into ADHD reflect a shift in the conceptualisation of this disorder from simple theoretical views of a few isolated dysfunctions to more complex models integrating the heterogeneity of the clinical manifestations of ADHD. Thus, findings from structural and functional neuroimaging suggest the involvement of developmentally abnormal brain networks related to cognition, attention, emotion and sensorimotor functions. Brain functioning alterations are confirmed by neurophysiological findings, showing that individuals with ADHD have elevated theta/beta power ratios, and less pronounced responses and longer latencies of event-related potentials, compared with controls. At a molecular level, alterations in any single neurotransmitter system are unlikely to explain the complexity of ADHD; rather, the disorder has been linked to dysfunctions in several systems, including the dopaminergic, adrenergic, serotoninergic and cholinergic pathways. Genetic studies showing a heritability of ∼60-75% suggest that a plethora of genes, each one with a small but significant effect, interact with environmental factors to increase the susceptibility to ADHD. Currently, findings from neurobiological research do not have a direct application in daily clinical practice, but it is hoped that in the near future they will complement the diagnostic process and contribute to the long-term effective treatment of this impairing condition.

AB - This review, addressed mainly to clinicians, considers commonly asked questions related to the neuroimaging, neurophysiology, neurochemistry and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD). It provides answers based on the most recent meta-analyses and systematic reviews, as well as additional relevant original studies. Empirical findings from neurobiological research into ADHD reflect a shift in the conceptualisation of this disorder from simple theoretical views of a few isolated dysfunctions to more complex models integrating the heterogeneity of the clinical manifestations of ADHD. Thus, findings from structural and functional neuroimaging suggest the involvement of developmentally abnormal brain networks related to cognition, attention, emotion and sensorimotor functions. Brain functioning alterations are confirmed by neurophysiological findings, showing that individuals with ADHD have elevated theta/beta power ratios, and less pronounced responses and longer latencies of event-related potentials, compared with controls. At a molecular level, alterations in any single neurotransmitter system are unlikely to explain the complexity of ADHD; rather, the disorder has been linked to dysfunctions in several systems, including the dopaminergic, adrenergic, serotoninergic and cholinergic pathways. Genetic studies showing a heritability of ∼60-75% suggest that a plethora of genes, each one with a small but significant effect, interact with environmental factors to increase the susceptibility to ADHD. Currently, findings from neurobiological research do not have a direct application in daily clinical practice, but it is hoped that in the near future they will complement the diagnostic process and contribute to the long-term effective treatment of this impairing condition.

KW - ADHD

KW - Genetics

KW - Neurobiology

KW - Neurochemistry

KW - Neuroimaging

KW - Neurophysiology

UR - http://www.scopus.com/inward/record.url?scp=84865125955&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84865125955&partnerID=8YFLogxK

U2 - 10.1016/j.ejpn.2012.01.009

DO - 10.1016/j.ejpn.2012.01.009

M3 - Article

VL - 16

SP - 422

EP - 433

JO - European Journal of Paediatric Neurology

JF - European Journal of Paediatric Neurology

SN - 1090-3798

IS - 5

ER -