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Attention-deficit-hyperactivity disorder and reward deficiency syndrome
Molecular genetic studies have identified several genes that may mediate susceptibility to attention deficit hyperactivity disorder (ADHD). A consensus of the literature suggests that when there is a dysfunction in the “brain reward cascade,” especially in the dopamine system, causing a low or hypo-...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626918/ https://www.ncbi.nlm.nih.gov/pubmed/19183781 |
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author | Blum, Kenneth Chen, Amanda Lih-Chuan Braverman, Eric R Comings, David E Chen, Thomas JH Arcuri, Vanessa Blum, Seth H Downs, Bernard W Waite, Roger L Notaro, Alison Lubar, Joel Williams, Lonna Prihoda, Thomas J Palomo, Tomas Oscar-Berman, Marlene |
author_facet | Blum, Kenneth Chen, Amanda Lih-Chuan Braverman, Eric R Comings, David E Chen, Thomas JH Arcuri, Vanessa Blum, Seth H Downs, Bernard W Waite, Roger L Notaro, Alison Lubar, Joel Williams, Lonna Prihoda, Thomas J Palomo, Tomas Oscar-Berman, Marlene |
author_sort | Blum, Kenneth |
collection | PubMed |
description | Molecular genetic studies have identified several genes that may mediate susceptibility to attention deficit hyperactivity disorder (ADHD). A consensus of the literature suggests that when there is a dysfunction in the “brain reward cascade,” especially in the dopamine system, causing a low or hypo-dopaminergic trait, the brain may require dopamine for individuals to avoid unpleasant feelings. This high-risk genetic trait leads to multiple drug-seeking behaviors, because the drugs activate release of dopamine, which can diminish abnormal cravings. Moreover, this genetic trait is due in part to a form of a gene (DRD(2) A1 allele) that prevents the expression of the normal laying down of dopamine receptors in brain reward sites. This gene, and others involved in neurophysiological processing of specific neurotransmitters, have been associated with deficient functions and predispose individuals to have a high risk for addictive, impulsive, and compulsive behavioral propensities. It has been proposed that genetic variants of dopaminergic genes and other “reward genes” are important common determinants of reward deficiency syndrome (RDS), which we hypothesize includes ADHD as a behavioral subtype. We further hypothesize that early diagnosis through genetic polymorphic identification in combination with DNA-based customized nutraceutical administration to young children may attenuate behavioral symptoms associated with ADHD. Moreover, it is concluded that dopamine and serotonin releasers might be useful therapeutic adjuncts for the treatment of other RDS behavioral subtypes, including addictions. |
format | Text |
id | pubmed-2626918 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-26269182009-02-01 Attention-deficit-hyperactivity disorder and reward deficiency syndrome Blum, Kenneth Chen, Amanda Lih-Chuan Braverman, Eric R Comings, David E Chen, Thomas JH Arcuri, Vanessa Blum, Seth H Downs, Bernard W Waite, Roger L Notaro, Alison Lubar, Joel Williams, Lonna Prihoda, Thomas J Palomo, Tomas Oscar-Berman, Marlene Neuropsychiatr Dis Treat Review Molecular genetic studies have identified several genes that may mediate susceptibility to attention deficit hyperactivity disorder (ADHD). A consensus of the literature suggests that when there is a dysfunction in the “brain reward cascade,” especially in the dopamine system, causing a low or hypo-dopaminergic trait, the brain may require dopamine for individuals to avoid unpleasant feelings. This high-risk genetic trait leads to multiple drug-seeking behaviors, because the drugs activate release of dopamine, which can diminish abnormal cravings. Moreover, this genetic trait is due in part to a form of a gene (DRD(2) A1 allele) that prevents the expression of the normal laying down of dopamine receptors in brain reward sites. This gene, and others involved in neurophysiological processing of specific neurotransmitters, have been associated with deficient functions and predispose individuals to have a high risk for addictive, impulsive, and compulsive behavioral propensities. It has been proposed that genetic variants of dopaminergic genes and other “reward genes” are important common determinants of reward deficiency syndrome (RDS), which we hypothesize includes ADHD as a behavioral subtype. We further hypothesize that early diagnosis through genetic polymorphic identification in combination with DNA-based customized nutraceutical administration to young children may attenuate behavioral symptoms associated with ADHD. Moreover, it is concluded that dopamine and serotonin releasers might be useful therapeutic adjuncts for the treatment of other RDS behavioral subtypes, including addictions. Dove Medical Press 2008-10 /pmc/articles/PMC2626918/ /pubmed/19183781 Text en © 2008 Dove Medical Press Limited. All rights reserved |
spellingShingle | Review Blum, Kenneth Chen, Amanda Lih-Chuan Braverman, Eric R Comings, David E Chen, Thomas JH Arcuri, Vanessa Blum, Seth H Downs, Bernard W Waite, Roger L Notaro, Alison Lubar, Joel Williams, Lonna Prihoda, Thomas J Palomo, Tomas Oscar-Berman, Marlene Attention-deficit-hyperactivity disorder and reward deficiency syndrome |
title | Attention-deficit-hyperactivity disorder and reward deficiency syndrome |
title_full | Attention-deficit-hyperactivity disorder and reward deficiency syndrome |
title_fullStr | Attention-deficit-hyperactivity disorder and reward deficiency syndrome |
title_full_unstemmed | Attention-deficit-hyperactivity disorder and reward deficiency syndrome |
title_short | Attention-deficit-hyperactivity disorder and reward deficiency syndrome |
title_sort | attention-deficit-hyperactivity disorder and reward deficiency syndrome |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626918/ https://www.ncbi.nlm.nih.gov/pubmed/19183781 |
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