Home > Publications database > Effects of a CACNA1C genotype on attention networks in healthy individuals. > print

001     16837
005     20210129210649.0
024 7 _ |2 pmid
|a pmid:21078228
024 7 _ |2 DOI
|a 10.1017/S0033291710002217
024 7 _ |2 WOS
|a WOS:000291854700022
037 _ _ |a PreJuSER-16837
041 _ _ |a eng
082 _ _ |a 610
084 _ _ |2 WoS
|a Psychology, Clinical
084 _ _ |2 WoS
|a Psychiatry
084 _ _ |2 WoS
|a Psychology
100 1 _ |0 P:(DE-HGF)0
|a Thimm, M.
|b 0
245 _ _ |a Effects of a CACNA1C genotype on attention networks in healthy individuals.
260 _ _ |a Cambridge
|b Cambridge Univ. Press
|c 2011
300 _ _ |a 1551 - 1561
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|0 0
|2 EndNote
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |0 24741
|a Psychological Medicine
|v 41
|y 7
500 _ _ |3 POF3_Assignment on 2016-02-29
500 _ _ |a This work was supported by the Federal Ministry of Education and Research (BMBF; Brain Imaging Centre West, 01GO0204 and 01GW0751) and by the START Program of the Medical Faculty of RWTH Aachen University.
520 _ _ |a Recent genetic studies found the A allele of the variant rs1006737 in the alpha 1C subunit of the L-type voltage-gated calcium channel (CACNA1C) gene to be over-represented in patients with psychosis, including schizophrenia, bipolar disorder and major depressive disorder. In these disorders, attention deficits are among the main cognitive symptoms and have been related to altered neural activity in cerebral attention networks. The particular effect of CACNA1C on neural function, such as attention networks, remains to be elucidated.The current event-related functional magnetic resonance imaging (fMRI) study investigated the effect of the CACNA1C gene on brain activity in 80 subjects while performing a scanner-adapted version of the Attention Network Test (ANT). Three domains of attention were probed simultaneously: alerting, orienting and executive control of attention.Risk allele carriers showed impaired performance in alerting and orienting in addition to reduced neural activity in the right inferior parietal lobule [Brodmann area (BA) 40] during orienting and in the medial frontal gyrus (BA 8) during executive control of attention. These areas belong to networks that have been related to impaired orienting and executive control mechanisms in neuropsychiatric disorders.Our results suggest that CACNA1C plays a role in the development of specific attention deficits in psychiatric disorders by modulation of neural attention networks.
536 _ _ |0 G:(DE-Juel1)FUEK255
|2 G:(DE-HGF)
|x 0
|c FUEK255
|a Neurowissenschaften (FUEK255)
536 _ _ |0 G:(DE-HGF)POF2-333
|a 333 - Pathophysiological Mechanisms of Neurological and Psychiatric Diseases (POF2-333)
|c POF2-333
|f POF II
|x 1
588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Adolescent
650 _ 2 |2 MeSH
|a Adult
650 _ 2 |2 MeSH
|a Attention: physiology
650 _ 2 |2 MeSH
|a Brain: physiology
650 _ 2 |2 MeSH
|a Calcium Channels, L-Type: genetics
650 _ 2 |2 MeSH
|a Cues
650 _ 2 |2 MeSH
|a Female
650 _ 2 |2 MeSH
|a Genotype
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Image Processing, Computer-Assisted
650 _ 2 |2 MeSH
|a Magnetic Resonance Imaging: methods
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Middle Aged
650 _ 2 |2 MeSH
|a Polymorphism, Single Nucleotide: genetics
650 _ 2 |2 MeSH
|a Reaction Time
650 _ 2 |2 MeSH
|a Reference Values
650 _ 2 |2 MeSH
|a Task Performance and Analysis
650 _ 2 |2 MeSH
|a Young Adult
650 _ 7 |0 0
|2 NLM Chemicals
|a CACNA1C protein, human
650 _ 7 |0 0
|2 NLM Chemicals
|a Calcium Channels, L-Type
650 _ 7 |2 WoSType
|a J
653 2 0 |2 Author
|a Alerting
653 2 0 |2 Author
|a executive control
653 2 0 |2 Author
|a fMRI
653 2 0 |2 Author
|a genetic imaging
653 2 0 |2 Author
|a orienting
653 2 0 |2 Author
|a psychiatric disorder
700 1 _ |0 P:(DE-HGF)0
|a Kircher, T.
|b 1
700 1 _ |0 P:(DE-HGF)0
|a Kellermann, T.
|b 2
700 1 _ |0 P:(DE-HGF)0
|a Markov, V.
|b 3
700 1 _ |0 P:(DE-HGF)0
|a Krach, S.
|b 4
700 1 _ |0 P:(DE-HGF)0
|a Jansen, A.
|b 5
700 1 _ |0 P:(DE-HGF)0
|a Zerres, K.
|b 6
700 1 _ |0 P:(DE-HGF)0
|a Eggermann, T.
|b 7
700 1 _ |0 P:(DE-Juel1)VDB18939
|a Stöcker, T.
|b 8
|u FZJ
700 1 _ |0 P:(DE-Juel1)131794
|a Shah, N.J.
|b 9
|u FZJ
700 1 _ |0 P:(DE-HGF)0
|a Nöthen, M.M.
|b 10
700 1 _ |0 P:(DE-HGF)0
|a Rietschel, M.
|b 11
700 1 _ |0 P:(DE-HGF)0
|a Witt, S.H.
|b 12
700 1 _ |0 P:(DE-Juel1)VDB1973
|a Mathiak, K.
|b 13
|u FZJ
700 1 _ |0 P:(DE-HGF)0
|a Krug, A.
|b 14
773 _ _ |0 PERI:(DE-600)1470300-2
|a 10.1017/S0033291710002217
|g Vol. 41, p. 1551 - 1561
|p 1551 - 1561
|q 41<1551 - 1561
|t Psychological medicine
|v 41
|x 0033-2917
|y 2011
856 7 _ |u http://dx.doi.org/10.1017/S0033291710002217
909 C O |o oai:juser.fz-juelich.de:16837
|p VDB
913 2 _ |a DE-HGF
|b Key Technologies
|l Decoding the Human Brain
|1 G:(DE-HGF)POF3-570
|0 G:(DE-HGF)POF3-579H
|2 G:(DE-HGF)POF3-500
|v Addenda
|x 0
913 1 _ |0 G:(DE-HGF)POF2-333
|1 G:(DE-HGF)POF2-330
|2 G:(DE-HGF)POF2-300
|a DE-HGF
|b Gesundheit
|l Funktion und Dysfunktion des Nervensystems
|v Pathophysiological Mechanisms of Neurological and Psychiatric Diseases
|x 3
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF2
914 1 _ |y 2011
915 _ _ |0 StatID:(DE-HGF)0010
|a JCR/ISI refereed
920 1 _ |0 I:(DE-Juel1)INM-4-20090406
|g INM
|k INM-4
|l Physik der Medizinischen Bildgebung
|x 0
920 1 _ |0 I:(DE-Juel1)INM-1-20090406
|g INM
|k INM-1
|l Strukturelle und funktionelle Organisation des Gehirns
|x 1
920 1 _ |0 I:(DE-Juel1)INM-5-20090406
|g INM
|k INM-5
|l Nuklearchemie
|x 2
970 _ _ |a VDB:(DE-Juel1)131146
980 _ _ |a VDB
980 _ _ |a ConvertedRecord
980 _ _ |a journal
980 _ _ |a I:(DE-Juel1)INM-4-20090406
980 _ _ |a I:(DE-Juel1)INM-1-20090406
980 _ _ |a I:(DE-Juel1)INM-5-20090406
980 _ _ |a UNRESTRICTED
981 _ _ |a I:(DE-Juel1)INM-1-20090406
981 _ _ |a I:(DE-Juel1)INM-5-20090406

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21