Attention-deficit/hyperactive disorder updates
Background Attention-deficit/hyperactive disorder (ADHD) is a neurodevelopmental disorder that commonly occurs in children with a prevalence ranging from 3.4 to 7.2%. It profoundly affects academic achievement, well-being, and social interactions. As a result, this disorder is of high cost to both i...
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Published in | Frontiers in molecular neuroscience Vol. 15; p. 925049 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Lausanne
Frontiers Research Foundation
21.09.2022
Frontiers Media S.A |
Subjects | |
Online Access | Get full text |
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Summary: | Background
Attention-deficit/hyperactive disorder (ADHD) is a neurodevelopmental disorder that commonly occurs in children with a prevalence ranging from 3.4 to 7.2%. It profoundly affects academic achievement, well-being, and social interactions. As a result, this disorder is of high cost to both individuals and society. Despite the availability of knowledge regarding the mechanisms of ADHD, the pathogenesis is not clear, hence, the existence of many challenges especially in making correct early diagnosis and provision of accurate management.
Objectives
We aimed to review the pathogenic pathways of ADHD in children. The major focus was to provide an update on the reported etiologies in humans, animal models, modulators, therapies, mechanisms, epigenetic changes, and the interaction between genetic and environmental factors.
Methods
References for this review were identified through a systematic search in PubMed by using special keywords for all years until January 2022.
Results
Several genes have been reported to associate with ADHD:
DRD1
,
DRD2
,
DRD4
,
DAT1
,
TPH2
,
HTR1A
,
HTR1B
,
SLC6A4
,
HTR2A
,
DBH
,
NET1
,
ADRA2A
,
ADRA2C
,
CHRNA4
,
CHRNA7
,
GAD1
,
GRM1
,
GRM5
,
GRM7
,
GRM8
,
TARBP1
,
ADGRL3
,
FGF1
,
MAOA
,
BDNF
,
SNAP25
,
STX1A
,
ATXN7
, and
SORCS2
. Some of these genes have evidence both from human beings and animal models, while others have evidence in either humans or animal models only. Notably, most of these animal models are knockout and do not generate the genetic alteration of the patients. Besides, some of the gene polymorphisms reported differ according to the ethnic groups. The majority of the available animal models are related to the dopaminergic pathway. Epigenetic changes including SUMOylation, methylation, and acetylation have been reported in genes related to the dopaminergic pathway.
Conclusion
The dopaminergic pathway remains to be crucial in the pathogenesis of ADHD. It can be affected by environmental factors and other pathways. Nevertheless, it is still unclear how environmental factors relate to all neurotransmitter pathways; thus, more studies are needed. Although several genes have been related to ADHD, there are few animal model studies on the majority of the genes, and they do not generate the genetic alteration of the patients. More animal models and epigenetic studies are required. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 These authors have contributed equally to this work Reviewed by: Matias Morin, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Spain; Jitendra Kumar Sinha, GloNeuro Academy, India This article was submitted to Brain Disease Mechanisms, a section of the journal Frontiers in Molecular Neuroscience Edited by: Michel J. Simonneau, École Normale Supérieure Paris-Saclay, France |
ISSN: | 1662-5099 1662-5099 |
DOI: | 10.3389/fnmol.2022.925049 |