Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate

C.A. Mastronardi, E. Pillai, D.A. Pineda, A.F. Martinez, F. Lopera, J.I. Velez, J.D. Palacio, H. Patel, S. Easteal, M.T. Acosta, F.X. Castellanos, M. Muenke, M. Arcos-Burgos

Resultado de la investigación: Contribución a una revistaArtículo

5 Citas (Scopus)

Resumen

Attention-deficit/hyperactivity disorder (ADHD) is a heritable, chronic, neurodevelopmental disorder with serious long-term repercussions. Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is based on subjective assessments of perceived behaviors. Endophenotypes (neurobiological markers that cosegregate and are associated with an illness) are thought to provide a more powerful and objective framework for revealing the underlying neurobiology than syndromic psychiatric classification. Here, we present the results of applying genetic linkage and association analyses to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms. We found several new genetic regions linked and/or associated with these endophenotypes, and others previously associated to ADHD, for example, loci harbored in the LPHN3, FGF1, POLR2A, CHRNA4 and ANKFY1 genes. These findings, when compared with those linked and/or associated to ADHD, suggest that these endophenotypes lie on shared pathways. The genetic information provided by this study offers a novel and complementary method of assessing the genetic causes underpinning the susceptibility to behavioral conditions and may offer new insights on the neurobiology of the disorder. © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.
Idioma originalInglés estadounidense
Páginas (desde-hasta)1434-1440
Número de páginas7
PublicaciónMolecular Psychiatry
Volumen21
N.º10
DOI
EstadoPublicada - 2016

Huella dactilar

Endophenotypes
Attention Deficit Disorder with Hyperactivity
Pedigree
Neurobiology
Fibroblast Growth Factor 1
Genetic Linkage
Microsatellite Repeats
Single Nucleotide Polymorphism
Psychiatry
Genes

Citar esto

Mastronardi, C. A., Pillai, E., Pineda, D. A., Martinez, A. F., Lopera, F., Velez, J. I., ... Arcos-Burgos, M. (2016). Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate. Molecular Psychiatry, 21(10), 1434-1440. https://doi.org/10.1038/mp.2015.172
Mastronardi, C.A. ; Pillai, E. ; Pineda, D.A. ; Martinez, A.F. ; Lopera, F. ; Velez, J.I. ; Palacio, J.D. ; Patel, H. ; Easteal, S. ; Acosta, M.T. ; Castellanos, F.X. ; Muenke, M. ; Arcos-Burgos, M. / Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate. En: Molecular Psychiatry. 2016 ; Vol. 21, N.º 10. pp. 1434-1440.
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abstract = "Attention-deficit/hyperactivity disorder (ADHD) is a heritable, chronic, neurodevelopmental disorder with serious long-term repercussions. Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is based on subjective assessments of perceived behaviors. Endophenotypes (neurobiological markers that cosegregate and are associated with an illness) are thought to provide a more powerful and objective framework for revealing the underlying neurobiology than syndromic psychiatric classification. Here, we present the results of applying genetic linkage and association analyses to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms. We found several new genetic regions linked and/or associated with these endophenotypes, and others previously associated to ADHD, for example, loci harbored in the LPHN3, FGF1, POLR2A, CHRNA4 and ANKFY1 genes. These findings, when compared with those linked and/or associated to ADHD, suggest that these endophenotypes lie on shared pathways. The genetic information provided by this study offers a novel and complementary method of assessing the genetic causes underpinning the susceptibility to behavioral conditions and may offer new insights on the neurobiology of the disorder. {\circledC} 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.",
author = "C.A. Mastronardi and E. Pillai and D.A. Pineda and A.F. Martinez and F. Lopera and J.I. Velez and J.D. Palacio and H. Patel and S. Easteal and M.T. Acosta and F.X. Castellanos and M. Muenke and M. Arcos-Burgos",
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Mastronardi, CA, Pillai, E, Pineda, DA, Martinez, AF, Lopera, F, Velez, JI, Palacio, JD, Patel, H, Easteal, S, Acosta, MT, Castellanos, FX, Muenke, M & Arcos-Burgos, M 2016, 'Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate', Molecular Psychiatry, vol. 21, n.º 10, pp. 1434-1440. https://doi.org/10.1038/mp.2015.172

Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate. / Mastronardi, C.A.; Pillai, E.; Pineda, D.A.; Martinez, A.F.; Lopera, F.; Velez, J.I.; Palacio, J.D.; Patel, H.; Easteal, S.; Acosta, M.T.; Castellanos, F.X.; Muenke, M.; Arcos-Burgos, M.

En: Molecular Psychiatry, Vol. 21, N.º 10, 2016, p. 1434-1440.

Resultado de la investigación: Contribución a una revistaArtículo

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T1 - Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate

AU - Mastronardi, C.A.

AU - Pillai, E.

AU - Pineda, D.A.

AU - Martinez, A.F.

AU - Lopera, F.

AU - Velez, J.I.

AU - Palacio, J.D.

AU - Patel, H.

AU - Easteal, S.

AU - Acosta, M.T.

AU - Castellanos, F.X.

AU - Muenke, M.

AU - Arcos-Burgos, M.

N1 - Cited By :1 Export Date: 4 April 2018 CODEN: MOPSF

PY - 2016

Y1 - 2016

N2 - Attention-deficit/hyperactivity disorder (ADHD) is a heritable, chronic, neurodevelopmental disorder with serious long-term repercussions. Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is based on subjective assessments of perceived behaviors. Endophenotypes (neurobiological markers that cosegregate and are associated with an illness) are thought to provide a more powerful and objective framework for revealing the underlying neurobiology than syndromic psychiatric classification. Here, we present the results of applying genetic linkage and association analyses to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms. We found several new genetic regions linked and/or associated with these endophenotypes, and others previously associated to ADHD, for example, loci harbored in the LPHN3, FGF1, POLR2A, CHRNA4 and ANKFY1 genes. These findings, when compared with those linked and/or associated to ADHD, suggest that these endophenotypes lie on shared pathways. The genetic information provided by this study offers a novel and complementary method of assessing the genetic causes underpinning the susceptibility to behavioral conditions and may offer new insights on the neurobiology of the disorder. © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.

AB - Attention-deficit/hyperactivity disorder (ADHD) is a heritable, chronic, neurodevelopmental disorder with serious long-term repercussions. Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is based on subjective assessments of perceived behaviors. Endophenotypes (neurobiological markers that cosegregate and are associated with an illness) are thought to provide a more powerful and objective framework for revealing the underlying neurobiology than syndromic psychiatric classification. Here, we present the results of applying genetic linkage and association analyses to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms. We found several new genetic regions linked and/or associated with these endophenotypes, and others previously associated to ADHD, for example, loci harbored in the LPHN3, FGF1, POLR2A, CHRNA4 and ANKFY1 genes. These findings, when compared with those linked and/or associated to ADHD, suggest that these endophenotypes lie on shared pathways. The genetic information provided by this study offers a novel and complementary method of assessing the genetic causes underpinning the susceptibility to behavioral conditions and may offer new insights on the neurobiology of the disorder. © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.

U2 - 10.1038/mp.2015.172

DO - 10.1038/mp.2015.172

M3 - Article

VL - 21

SP - 1434

EP - 1440

JO - Molecular Psychiatry

JF - Molecular Psychiatry

SN - 1359-4184

IS - 10

ER -