Interactive effects of APOE and CHRNA4 on attention and white matter volume in healthy middle-aged and older adults

Espeseth, Thomas; Greenwood, Pamela M.; Reinvang, Ivar; Fjell, Anders M.; Walhovd, Kristine B.; Westlye, Lars T.; Wehling, Eike; Lundervold, Astri J.; Rootwelt, Helge; Parasuraman, Raja

doi:10.3758/cabn.6.1.31

Cited by 81 publications

(89 citation statements)

References 77 publications

(81 reference statements)

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“…Analysis of the effect of APOE on white matter volume and cortical thickness has been published by Espeseth et al (2006Espeseth et al ( , 2008. Further, Espeseth et al (2012) link APOE-related changes of cortical thickness to variation in attention.…”

Section: Mri-based Imagingmentioning

confidence: 99%

“…The task is to make a vowel/consonant discrimination on this letter. See Espeseth et al (2006) for details on this particular version. Measures endogenous covert visuo-spatial orienting and reorienting, phasic alertness.…”

Section: Appendixmentioning

confidence: 99%

“…In this context the NCNG is a comparatively large sample with a broad range of paradigms, and we will use the GWA study data on NCNG and collaborating replication samples to attempt a genetic parsing of attentional components. Based on the studies by Greenwood and Parasuraman (2003), we selected the Cued Discrimination paradigm as the measure of visual attention in the basic protocol (for details, see Espeseth et al, 2006). This is a version of the extensively studied paradigm originally developed by Posner (1980), where centrally located arrows give a neutral, valid, or invalid cue to the location of peripherally presented visual targets.…”

Section: The Genetics Of Experimental Cognitive Psychology Tasksmentioning

confidence: 99%

“…Due to the original aims of the NCNG Project, genotype data is available for APOE, CHRNA4, and a selection of DNA repair and neuronal plasticity genes for a subset of the sample, as described in Espeseth et al (2006), Le Hellard et al (2009), andLillenes et al (2011). For the GWA study, NCNG DNA samples were freshly extracted from blood and genotyped on the Illumina Human610-Quad Beadchip.…”

Section: Genotyping and Population Structurementioning

confidence: 99%

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Imaging and Cognitive Genetics: The Norwegian Cognitive NeuroGenetics Sample

et al. 2012

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Data collection for the Norwegian Cognitive NeuroGenetics sample (NCNG) was initiated in 2003 with a research grant (to Ivar Reinvang) to study cognitive aging, brain function, and genetic risk factors. The original focus was on the effects of aging (from middle age and up) and candidate genes (e.g., APOE, CHRNA4) in cross-sectional and longitudinal designs, with the cognitive and MRI-based data primarily being used for this purpose. However, as the main topic of the project broadened from cognitive aging to imaging and cognitive genetics more generally, the sample size, age range of the participants, and scope of available phenotypes and genotypes, have developed beyond the initial project. In 2009, a genome-wide association (GWA) study was undertaken, and the NCNG proper was established to study the genetics of cognitive and brain function more comprehensively. The NCNG is now controlled by the NCNG Study Group, which consists of the present authors. Prominent features of the NCNG are the adult life-span coverage of healthy participants with high-dimensional imaging, and cognitive data from a genetically homogenous sample. Another unique property is the large-scale (sample size 300-700) use of experimental cognitive tasks focusing on attention and working memory. The NCNG data is now used in numerous ongoing GWA-based studies and has contributed to several international consortia on imaging and cognitive genetics. The objective of the following presentation is to give other researchers the information necessary to evaluate possible contributions from the NCNG to various multi-sample data analyses.

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Section: Mri-based Imagingmentioning

confidence: 99%

Section: Appendixmentioning

confidence: 99%

Section: The Genetics Of Experimental Cognitive Psychology Tasksmentioning

confidence: 99%

Section: Genotyping and Population Structurementioning

confidence: 99%

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Imaging and Cognitive Genetics: The Norwegian Cognitive NeuroGenetics Sample

et al. 2012

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“…Karmiloff-Smith argues that "because ontogenetic development and timing play such important roles in development, a tiny impairment in the start state of the brain of a child with a genetic disorder may affect several brain regions, some more profoundly and others more subtly, giving rise in the phenotypic endstate to what appears to be a domain-specific outcome" (p. xxx). It is important to keep this neuroconstructivist perspective in mind when one is interpreting simple genebehavior associations in developmental disorders such as those described by Waldman et al (2006) and by Espeseth et al (2006) in this issue.…”

Section: Putting Genetic Variant and Phenotype Together: What Are Thementioning

confidence: 99%

Genes, brain, and behavior: Bridging disciplines

Fossella

Casey

2006

Cognitive, Affective, & Behavioral Neuroscience

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Risk gene variants for nicotine dependence in the CHRNA5–CHRNA3–CHRNB4 cluster are associated with cognitive performance

Winterer

Mittelstraß

Giegling

et al. 2010

American J of Med Genetics Pt B

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Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5-CHRNA3-CHRNB4 with nicotine dependence (ND). However, the precise genotype-phenotype relationship is still unknown. Clinical and epidemiological data on smoking behavior raise the possibility that the relevant gene variants may indirectly contribute to the development of ND by affecting cognitive performance in some smokers who consume nicotine for reasons of "cognition enhancement." Here, we tested seven single nucleotide polymorphisms (SNPs) rs684513, rs637137, rs16969968, rs578776, rs1051730, rs3743078, rs3813567 from the CHRNA5-CHRNA3-CHRNB4 gene cluster for association with ND, measures of cognitive performance and gene expression. As expected, we found all SNPs being associated with ND in three independent cohorts (KORA, NCOOP, ESTHER) comprising 5,561 individuals. In an overlapping sample of 2,186 subjects we found three SNPs (rs16969968, rs1051730, rs3743078) being associated with cognitive domains from the Wechsler-Adult-Intelligence Scale (WAIS-R)-most notably in the performance subtest "object assembly" and the verbal subtest "similarities." In a refined analysis of a subsample of 485 subjects, two of these three SNPs (rs16969968, rs1051730) were associated with n-back task performance/Continuous Performance Test. Furthermore, two CHRNA5 risk alleles (rs684513, rs637137) were associated with CHRNA5 mRNA expression levels in whole blood in a subgroup of 190 subjects. We here report for the first time an association of CHRNA5-CHRNA3-CHRNB4 gene variants with cognition possibly mediating in part risk for developing ND. The observed phenotype-genotype associations may depend on altered levels of gene expression. © 2010 Wiley-Liss, Inc.

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Interactive effects of APOE and CHRNA4 on attention and white matter volume in healthy middle-aged and older adults

Cited by 81 publications

References 77 publications

Imaging and Cognitive Genetics: The Norwegian Cognitive NeuroGenetics Sample

Imaging and Cognitive Genetics: The Norwegian Cognitive NeuroGenetics Sample

Genes, brain, and behavior: Bridging disciplines

Risk gene variants for nicotine dependence in the CHRNA5–CHRNA3–CHRNB4 cluster are associated with cognitive performance

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