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Status: Bibliographieeintrag

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Verfasst von:Erk, Susanne [VerfasserIn]   i
 Meyer-Lindenberg, Andreas [VerfasserIn]   i
 Schnell, Knut [VerfasserIn]   i
 Opitz von Boberfeld, Carola [VerfasserIn]   i
 Esslinger, Christine [VerfasserIn]   i
 Kirsch, Peter [VerfasserIn]   i
 Grimm, Oliver [VerfasserIn]   i
 Arnold, Claudia [VerfasserIn]   i
 Haller, Leila [VerfasserIn]   i
 Witt, Stephanie [VerfasserIn]   i
 Cichon, Sven [VerfasserIn]   i
 Nöthen, Markus M. [VerfasserIn]   i
 Rietschel, Marcella [VerfasserIn]   i
 Walter, Henrik [VerfasserIn]   i
Titel:Brain function in carriers of a genome-wide supported bipolar disorder variant
Verf.angabe:Susanne Erk, Andreas Meyer-Lindenberg, Knut Schnell, Carola Opitz von Boberfeld, Christine Esslinger, Peter Kirsch, Oliver Grimm, Claudia Arnold, Leila Haddad, Stephanie H. Witt, Sven Cichon, Markus M. Nöthen, Marcella Rietschel, Henrik Walter
E-Jahr:2010
Jahr:August 2010
Umfang:9 S.
Fussnoten:Gesehen am 25.05.2023
Titel Quelle:Enthalten in: Archives of general psychiatry
Ort Quelle:Chicago, Ill. : AMA, 1959
Jahr Quelle:2010
Band/Heft Quelle:67(2010), 8 vom: Aug., Seite 803-811
ISSN Quelle:1538-3636
Abstract:The neural abnormalities underlying genetic risk for bipolar disorder, a severe, common, and highly heritable psychiatric condition, are largely unknown. An opportunity to define these mechanisms is provided by the recent discovery, through genome-wide association, of a single-nucleotide polymorphism (rs1006737) strongly associated with bipolar disorder within the CACNA1C gene, encoding the α subunit of the L-type voltage-dependent calcium channel Cav1.2.To determine whether the genetic risk associated with rs1006737 is mediated through hippocampal function.Functional magnetic resonance imaging study.University hospital.A total of 110 healthy volunteers of both sexes and of German descent in the Hardy-Weinberg equilibrium for rs1006737.Blood oxygen level-dependent signal during an episodic memory task and behavioral and psychopathological measures.Using an intermediate phenotype approach, we show that healthy carriers of the CACNA1C risk variant exhibit a pronounced reduction of bilateral hippocampal activation during episodic memory recall and diminished functional coupling between left and right hippocampal regions. Furthermore, risk allele carriers exhibit activation deficits of the subgenual anterior cingulate cortex, a region repeatedly associated with affective disorders and the mediation of adaptive stress-related responses. The relevance of these findings for affective disorders is supported by significantly higher psychopathology scores for depression, anxiety, obsessive-compulsive thoughts, interpersonal sensitivity, and neuroticism in risk allele carriers, correlating negatively with the observed regional brain activation.Our data demonstrate that rs1006737 or genetic variants in linkage disequilibrium with it are functional in the human brain and provide a neurogenetic risk mechanism for bipolar disorder backed by genome-wide evidence.
DOI:doi:10.1001/archgenpsychiatry.2010.94
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1001/archgenpsychiatry.2010.94
 DOI: https://doi.org/10.1001/archgenpsychiatry.2010.94
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1846216834
Verknüpfungen:→ Zeitschrift

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