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000016837 084__ $$2WoS$$aPsychology, Clinical
000016837 084__ $$2WoS$$aPsychiatry
000016837 084__ $$2WoS$$aPsychology
000016837 1001_ $$0P:(DE-HGF)0$$aThimm, M.$$b0
000016837 245__ $$aEffects of a CACNA1C genotype on attention networks in healthy individuals.
000016837 260__ $$aCambridge$$bCambridge Univ. Press$$c2011
000016837 300__ $$a1551 - 1561
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000016837 440_0 $$024741$$aPsychological Medicine$$v41$$y7
000016837 500__ $$3POF3_Assignment on 2016-02-29
000016837 500__ $$aThis 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.
000016837 520__ $$aRecent genetic studies found the A allele of the variant rs1006737 in the alpha 1C subunit of the L-type voltage-gated calcium channel (CACNA1C) gene to be over-represented in patients with psychosis, including schizophrenia, bipolar disorder and major depressive disorder. In these disorders, attention deficits are among the main cognitive symptoms and have been related to altered neural activity in cerebral attention networks. The particular effect of CACNA1C on neural function, such as attention networks, remains to be elucidated.The current event-related functional magnetic resonance imaging (fMRI) study investigated the effect of the CACNA1C gene on brain activity in 80 subjects while performing a scanner-adapted version of the Attention Network Test (ANT). Three domains of attention were probed simultaneously: alerting, orienting and executive control of attention.Risk allele carriers showed impaired performance in alerting and orienting in addition to reduced neural activity in the right inferior parietal lobule [Brodmann area (BA) 40] during orienting and in the medial frontal gyrus (BA 8) during executive control of attention. These areas belong to networks that have been related to impaired orienting and executive control mechanisms in neuropsychiatric disorders.Our results suggest that CACNA1C plays a role in the development of specific attention deficits in psychiatric disorders by modulation of neural attention networks.
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000016837 65320 $$2Author$$aAlerting
000016837 65320 $$2Author$$aexecutive control
000016837 65320 $$2Author$$afMRI
000016837 65320 $$2Author$$agenetic imaging
000016837 65320 $$2Author$$aorienting
000016837 65320 $$2Author$$apsychiatric disorder
000016837 650_2 $$2MeSH$$aAdolescent
000016837 650_2 $$2MeSH$$aAdult
000016837 650_2 $$2MeSH$$aAttention: physiology
000016837 650_2 $$2MeSH$$aBrain: physiology
000016837 650_2 $$2MeSH$$aCalcium Channels, L-Type: genetics
000016837 650_2 $$2MeSH$$aCues
000016837 650_2 $$2MeSH$$aFemale
000016837 650_2 $$2MeSH$$aGenotype
000016837 650_2 $$2MeSH$$aHumans
000016837 650_2 $$2MeSH$$aImage Processing, Computer-Assisted
000016837 650_2 $$2MeSH$$aMagnetic Resonance Imaging: methods
000016837 650_2 $$2MeSH$$aMale
000016837 650_2 $$2MeSH$$aMiddle Aged
000016837 650_2 $$2MeSH$$aPolymorphism, Single Nucleotide: genetics
000016837 650_2 $$2MeSH$$aReaction Time
000016837 650_2 $$2MeSH$$aReference Values
000016837 650_2 $$2MeSH$$aTask Performance and Analysis
000016837 650_2 $$2MeSH$$aYoung Adult
000016837 650_7 $$00$$2NLM Chemicals$$aCACNA1C protein, human
000016837 650_7 $$00$$2NLM Chemicals$$aCalcium Channels, L-Type
000016837 650_7 $$2WoSType$$aJ
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000016837 7001_ $$0P:(DE-HGF)0$$aMarkov, V.$$b3
000016837 7001_ $$0P:(DE-HGF)0$$aKrach, S.$$b4
000016837 7001_ $$0P:(DE-HGF)0$$aJansen, A.$$b5
000016837 7001_ $$0P:(DE-HGF)0$$aZerres, K.$$b6
000016837 7001_ $$0P:(DE-HGF)0$$aEggermann, T.$$b7
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000016837 7001_ $$0P:(DE-HGF)0$$aKrug, A.$$b14
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