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Chagnon, Yvon C.

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Chagnon

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Yvon C.

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Université Laval. Département de psychiatrie et de neurosciences

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Voici les éléments 1 - 10 sur 13
  • PublicationAccès libre
    Relationship between cortisol level and prevalent/incident cognitive impairment and its moderating factors in older adults
    (Cambridge University Press, 2012-10-23) Potvin, Olivier; Forget, Hélène; Chagnon, Yvon C.; Préville, Michel; Hudon, Carol; Berbiche, Djamal
    Background : The objectives of this study were to examine the factors modifying the relationship between cortisol level and prevalent/incident cognitive impairment in older adults and to verify whether these relationships were non-linear. Methods : Data were collected from 1,226 individuals aged 65 and older by two in-home interviews separated by 12 months. Cortisol level was measured using saliva samples taken at the beginning of the baseline interview before cognitive, mental, and physical health evaluations. Prevalent and incident cognitive impairment were defined using the Mini-Mental State Examination scores according to normative data for age, education level, and sex. Results : High morning cortisol level increased the risk of incident cognitive impairment in participants with anxiety or depressive episode while low cortisol level increased the risk in participants without anxiety or depressive episode. In high educated participants, but not in low educated participants, high morning cortisol level was associated with prevalent cognitive impairment and high afternoon cortisol level increased the risk of incident cognitive impairment. The results also suggested that lower morning cortisol values could increase the risk of incident cognitive impairment in individuals with few chronic diseases. A curvilinear relationship was observed between morning cortisol and the probability of incident cognitive impairment, but further analyses suggested that it was likely explained by anxiety and depressive episode. Conclusions : These results suggest that cognitive impairment in older adults is linked to higher or lower cortisol level depending on characteristics such as anxiety, depressive episode, education level, and physical health.
  • PublicationAccès libre
    Genome-wide linkage scan reveals multiple susceptibility loci influencing lipid and lipoprotein levels in the Québec Family Study
    (American Society for Biochemistry et Molecular Biology, Inc., 2003-12-16) Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Rice, Treva; Bossé, Yohan; Rao, D. C. (Dabeeru C.); Vohl, Marie-Claude; Després, Jean-Pierre
    A genome-wide linkage study was performed to identify chromosomal regions harboring genes influencing lipid and lipoprotein levels. Linkage analyses were conducted for four quantitative lipoprotein/lipid traits, i.e., total cholesterol, triglyceride, HDL-cholesterol (HDL-C), and LDL-C concentrations, in 930 subjects enrolled in the Québec Family Study. A maximum of 534 pairs of siblings from 292 nuclear families were available. Linkage was tested using both allele-sharing and variance-component linkage methods. The strongest evidence of linkage was found on chromosome 12q14.1 at marker D12S334 for HDL-C, with a logarithm of the odds (LOD) score of 4.06. Chromosomal regions harboring quantitative trait loci (QTLs) for LDL-C included 1q43 (LOD = 2.50), 11q23.2 (LOD = 3.22), 15q26.1 (LOD = 3.11), and 19q13.32 (LOD = 3.59). In the case of triglycerides, three markers located on 2p14, 11p13, and 11q24.1 provided suggestive evidence of linkage (LOD > 1.75). Tests for total cholesterol levels yielded significant evidence of linkage at 15q26.1 and 18q22.3 with the allele-sharing linkage method, but the results were nonsignificant with the variance-component method. In conclusion, this genome scan provides evidence for several QTLs influencing lipid and lipoprotein levels. Promising candidate genes were located in the vicinity of the genomic regions showing evidence of linkage.
  • PublicationRestreint
    Evidence for a major quantitative trait locus on chromosome 17q21 affecting low-density lipoprotein peak particle diameter
    (Grune & Stratton, 2003-05-05) Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Lamarche, Benoît; Bossé, Yohan; Rice, Treva; Vohl, Marie-Claude; Rao, D. C. (Dabeeru C.); Després, Jean-Pierre
    Background— Several lines of evidence suggest that small dense LDL particles are associated with the risk of coronary heart disease. Heritability and segregation studies suggest that LDL particle size is characterized by a large genetic contribution and the presence of a putative major genetic locus. However, association and linkage analyses have thus far been inconclusive in identifying the underlying gene(s). Methods and Results— An autosomal genome-wide scan for LDL peak particle diameter (LDL-PPD) was performed in the Québec Family Study. A total of 442 markers were genotyped, with an average intermarker distance of 7.2 cM. LDL-PPD was measured by gradient gel electrophoresis in 681 subjects from 236 nuclear families. Linkage was tested by both sib-pair–based and variance components–based linkage methods. The strongest evidence of linkage was found on chromosome 17q21.33 at marker D17S1301, with an LOD score of 6.76 by the variance-components method for the phenotype adjusted for age, body mass index, and triglyceride levels. Similar results were obtained with the sib-pair method (P<0.0001). Other chromosomal regions harboring markers with highly suggestive evidence of linkage (P≤0.0023; LOD ≥1.75) include 1p31, 2q33.2, 4p15.2, 5q12.3, and 14q31. Several candidate genes are localized under the peak linkages, including apolipoprotein H on chromosome 17q, the apolipoprotein E receptor 2, and members of the phospholipase A2 family on chromosome 1p as well as HMG-CoA reductase on chromosome 5q. Conclusions— This genome-wide scan for LDL-PPD indicates the presence of a major quantitative trait locus located on chromosome 17q and others interesting loci influencing the phenotype.
  • PublicationAccès libre
    A multimodal attempt to follow-up linkage regions using RNA expression, SNPs and CpG methylation in schizophrenia and bipolar disorder kindreds
    (European Society of Human Genetics, 2019-11-06) Croteau, Jordie; Chagnon, Yvon C.; Paccalet, Thomas; Roy, Marc-André; Fournier, Alain; Bureau, Alexandre; Maziade, Michel
    The complexity of schizophrenia (SZ) and bipolar disorder (BD) has slowed down progress in understanding their genetic roots. Alternative genomic approaches are needed to bypass these difficulties. We attempted a multimodal approach to follow-up on reported linkage findings in SZ and BD from the Eastern Quebec kindreds in chromosomes 3q21, 4p34, 6p22, 8p21, 8p11, 13q11-q14, 15q13, 16p12, and 18q21. First, in 498 subjects, we measured RNA expression (47 K Illumina chips) in SZ and BD patients that we compared with their non-affected relatives (NARs) to identify, for each chromosomal region, genes showing the most significant differences in expression. Second, we performed SNP genotyping (700 K Illumina chips) and cis-eQTN analysis. Third, we measured DNA methylation on genes with RNA expression differences or eQTNs. We found a significant overexpression of the gene ITGB5 at 3q25 in SZ and BD after multiple testing p value adjustment. SPCS3 gene at 4q34, and FZD3 gene at 8p21, contained significant eQTNs after multiple testing corrections, while ITGB5 provided suggestive results. Methylation in associated genes did not explain the expression differences between patients and NARs. Our multimodal approach involving RNA expression, dense SNP genotyping and eQTN analyses, restricted to chromosomal regions having shown linkage, lowered the multiple testing burden and allowed for a deeper examination of candidate genes in SZ or BD.
  • PublicationAccès libre
    The interaction of GSK3B and FXR1 genotypes may influence the mania and depression dimensions in mood disorders
    (Elsevier, 2017-02-16) Beaulieu, Jean Martin; Chagnon, Yvon C.; Paccalet, Thomas; Bureau, Alexandre; Maziade, Michel
    Background: Previous evidence in healthy subjects suggested that functional polymorphisms GSK3B rs12630592 and FXR1 rs496250 interact in regulating mood and emotional processing. We attempted to replicate this interaction primarily on manic and depressive dimensions in mood disorder patients, and secondarily on schizophrenia patients, diagnosis itself and age of onset. Methods : Symptom dimensions were derived from the Comprehensive Assessment of Symptoms and History 82 items rated lifetime in acute episodes and stabilized interepisode intervals in 384 patients from the Schizophrenia and Bipolar Disorder Eastern Quebec Kindred Study. Linear mixed effect models of symptom dimensions included rs12630592-rs496250 main and interaction fixed effects (obtained from TaqMan genotypes), and a polygenic random effect. The distribution of lifetime best-estimate DSM-IV diagnosis of 855 kindred members was studied versus genotype under a polytomous logistic model. Results : In mood disorder patients, the level of mania (in both acute and stabilized periods) and depression in stabilized periods was positively associated with GSK3B rs12630592 T only in FXR1 rs496250 A-allele carriers (Bonferroni-corrected interaction p=0.024, 0.052 and 0.017 respectively). The two polymorphisms explained 11% of mania variance and 5% of interepisode depression variance. The association was observed neither in schizophrenia patients nor with the psychotic dimension in mood disorder patients. Interaction with the diagnosis distribution (p=0.03) was driven by the decreasing prevalence of recurrent major depression with rs12630592 T also only in carriers of rs496250 A. Limitations : Sample size was limited, but power was sufficient to detect the tested interaction effect in this replication sample. Conclusions : We replicate in affective patients an interaction between the FXR1 rs496250 and GSK3B rs12630592 polymorphisms in regulating mood dimensions.
  • PublicationRestreint
    Abdominal visceral fat is associated with a BclI restriction fragment length polymorphism at the glucocorticoid receptor gene locus
    (North American Association for the Study of Obesity, 1997-05-01) Buemann, Benjamin; Bouchard, Claude; Dionne, France T.; Chagnon, Monique; Chagnon, Yvon C.; Pérusse, Louis; Nadeau, André; Gagnon, Jacques; Tremblay, Angelo; Vohl, Marie-Claude; Després, Jean-Pierre
    Several investigations have suggested that body fat distribution is influenced by nonpathologic variations in the responsiveness to Cortisol. Genetic variations in the glucocorticoid receptor (GRL) could therefore potentially have an impact on the level of abdominal fat. A restriction fragment length polymorphism (RFLP) has previously been detected with the BelI restriction enzyme in the GRL gene identifying two alleles with fragment lengths of 4.5 and 2.3 kb. This study investigates whether abdominal fat areas measured by computerized tomography (CT) are associated with this polymorphism in 152 middle-aged men and women. The less frequent 4.5-kb allele was found to be associated with a higher abdominal visceral fat (A VF) area independently of total body fat mass (4.5/4.5 vs. 2.3/2.3 kb genotype; men: 190.7 ± 30.1 vs. 150.7 ± 33.3 cm2, p=0.04; women: 132.7 ± 37.3 vs. 101.3 ± 34.5 cm2, p=0.06). However, the association with AVF was seen only in subjects of the lower tertile of the percent body fat level. In these subjects, the polymorphism was found to account for 41% (p=0.003) and 35% (p=0.007), in men and women, respectively, of the total variance in AVF area. The consistent association between the GRL polymorphism detected with BelI and AVF area suggests that this gene or a locus in linkage disequilibrium with the BelI restriction site may contribute to the accumulation of AVF.
  • PublicationAccès libre
    Compendium of genome-wide scans of lipid-related phenotypes : adding a new genome-wide search of apolipoproteins levels
    (American Society for Biochemistry and Molecular Biology, 2004-09-16) Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Rice, Treva; Bossé, Yohan; Rao, D. C.; Vohl, Marie-Claude; Després, Jean-Pierre
    The genetic dissection of complex inherited diseases is a major challenge. Despite limited success in finding genes, substantial data based on genome-wide scan strategies is now available for a variety of diseases and related phenotypes. This can perhaps best be appreciated in the field of lipid and lipoprotein levels, where the amount of information generated is becoming overwhelming. We have created a database containing the results from whole-genome scans of lipid-related phenotypes undertaken to date. The usefulness of this database is demonstrated by performing a new autosomal genomic scan on apolipoprotein B (apoB), LDL-apoB, and apoA-I levels, measured in 679 subjects of 243 nuclear families. Linkage was tested using both allele-sharing and variance-component methods. Only two loci provided support for linkage with both methods: a LDL-apoB locus on 18q21.32 and an apoA-I locus on 3p25.2. Adding those findings to the database highlighted the fact that the former is reported as a lipid-related locus for the first time, whereas the latter has been observed before. However, concerns arise when displaying all data on the same map, because a large portion of the genome is now covered with loci supported by at least suggestive evidence of linkage.
  • PublicationRestreint
    Neuromedin β : a strong candidate gene linking eating behaviors and susceptibility to obesity
    (Journal of Clinical Nutrition, 2004-01-01) Drapeau, Vicky; Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Tremblay, Angelo; Rice, Treva; Lemieux, Simone; Rao, D. C. (Dabeeru C.); Vohl, Marie-Claude; Bouchard, Luigi; Provencher, Véronique
    Background: Obesity is frequently associated with eating disorders, and evidence indicates that both conditions are influenced by genetic factors. However, little is known about the genes influencing eating behaviors. Objective: The objective was to identify genes associated with eating behaviors. Design: Three eating behaviors were assessed in 660 adults from the Québec Family Study with the use of the Three-Factor Eating Questionnaire. A genome-wide scan was conducted with a total of 471 genetic markers spanning the 22 autosomes to identify quantitative trait loci for eating behaviors. Body composition and macronutrient and energy intakes were also measured. Results: Four quantitative trait loci were identified for disinhibition and susceptibility to hunger. Of these, the best evidence of linkage was found between a locus on chromosome 15q24-q25 and disinhibition (P < 0.0058) and susceptibility to hunger (P < 0.0001). After fine-mapping, the peak linkage was found between markers D15S206 and D15S201 surrounding the neuromedin β (NMB) gene. A missense mutation (p.P73T) located within the NMB gene showed significant associations with eating behaviors and obesity phenotypes. The T73T homozygotes were 2 times as likely to exhibit high levels of disinhibition (odds ratio: 1.8; 95% CI: 1.07, 2.89; P = 0.03) and susceptibility to hunger (odds ratio: 1.9; 95% CI: 1.15, 3.06; P = 0.01) as were the P73 allele carriers. Six-year follow-up data showed that the amount of body fat gain over time in T73T subjects was >2 times that than in P73P homozygotes (3.6 compared with 1.5 kg; P < 0.05
  • PublicationRestreint
    Measuring how genetic and epigenetic variants can filter emotion perception
    (Clinical Neuroscience Publishers, 2015-10-01) Hétu, Sébastien; Jackson, Philip L.; Taschereau-Dumouchel, Vincent; Chagnon, Yvon C.
    Emotion perception has been extensively studied in cognitive neurosciences and stands as a promising intermediate phenotype of social cognitive processes and psychopathologies. Exciting imaging genetic studies have recently identified genetic and epigenetic variants affecting brain responses during emotion perception tasks, but characterizing how these variants interact and relate to higher-order cognitive processes remains a challenge. Here, we integrate works in parallel fields and propose a new psychophysical conceptualization to address this issue. This approach proposes to consider genetic variants as ‘filters’ of perceptual information that can interact to shape different perceptual profiles. Importantly, these perceptual profiles can be precisely described and compared between multivariate genetic groups using a new psychophysical method. Crucially, this approach represents a potentially powerful novel tool to address gene-by-gene and gene-by-environment interactions, and provides a new cognitive perspective to link social perceptive and social cognitive processes in the context of psychiatric disorders.
  • PublicationAccès libre
    BDNF Val66Met polymorphism is associated with self-reported empathy
    (Public Library of Science, 2016-02-22) Hétu, Sébastien; Jackson, Philip L.; Taschereau-Dumouchel, Vincent; Chagnon, Yvon C.; Bagramyan, Anaït; Labrecque, Alexandre; Racine, Marion
    Empathy is an important driver of human social behaviors and presents genetic roots that have been studied in neuroimaging using the intermediate phenotype approach. Notably, the Val66Met polymorphism of the Brain-derived neurotrophic factor (BDNF) gene has been identified as a potential target in neuroimaging studies based on its influence on emotion perception and social cognition, but its impact on self-reported empathy has never been documented. Using a neurogenetic approach, we investigated the association between the BDNF Val66Met polymorphism and self-reported empathy (Davis’ Interpersonal Reactivity Index; IRI) in a sample of 110 young adults. Our results indicate that the BDNF genotype is significantly associated with the linear combination of the four facets of the IRI, one of the most widely used self-reported empathy questionnaire. Crucially, the effect of BDNF Val66Met goes beyond the variance explained by two polymorphisms of the oxytocin transporter gene previously associated with empathy and its neural underpinnings (OXTR rs53576 and rs2254298). These results represent the first evidence suggesting a link between the BDNF gene and self-reported empathy and warrant further studies of this polymorphism due to its potential clinical significance.