👤 C Berr

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2
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Also published as: Claudine Berr
articles
Olav M Andersen, Matthijs W J de Waal, Giulia Monti +103 more · 2025 · Molecular neurodegeneration · BioMed Central · added 2026-04-24
Olav M Andersen, Matthijs W J de Waal, Giulia Monti, Niccolo Tesi, Anne Mette G Jensen, Christa de Geus, Rosalina van Spaendonk, Maartje Vogel, Shahzad Ahmad, Najaf Amin, Philippe Amouyel, Gary W Beecham, Céline Bellenguez, Claudine Berr, Joshua C Bis, Anne Boland, Paola Bossù, Femke Bouwman, Jose Bras, Camille Charbonnier, Jordi Clarimon, Carlos Cruchaga, Antonio Daniele, Jean-François Dartigues, Stéphanie Debette, Jean-François Deleuze, Nicola Denning, Anita L Destefano, Oriol Dols-Icardo, Cornelia M Van Duijn, Lindsay A Farrer, Maria Victoria Fernández, Wiesje M van der Flier, Nick C Fox, Daniela Galimberti, Emmanuelle Genin, Johan J P Gille, Benjamin Grenier-Boley, Detelina Grozeva, Yann Le Guen, Rita Guerreiro, Jonathan L Haines, Clive Holmes, Holger Hummerich, M Arfan Ikram, M Kamran Ikram, Amit Kawalia, Robert Kraaij, Jean-Charles Lambert, Marc Lathrop, Afina W Lemstra, Alberto Lleó, Richard M Myers, Marcel M A M Mannens, Rachel Marshall, Eden R Martin, Carlo Masullo, Richard Mayeux, Simon Mead, Patrizia Mecocci, Alun Meggy, Merel O Mol, Benedetta Nacmias, Adam C Naj, Valerio Napolioni, J Nicholas Cochran, Gaël Nicolas, Florence Pasquier, Pau Pastor, Margaret A Pericak-Vance, Yolande A L Pijnenburg, Fabrizio Piras, Olivier Quenez, Alfredo Ramirez, Rachel Raybould, Richard Redon, Marcel J T Reinders, Anne-Claire Richard, Steffi G Riedel-Heller, Fernando Rivadeneira, Jeroen G J van Rooij, Stéphane Rousseau, Natalie S Ryan, Pascual Sanchez-Juan, Gerard D Schellenberg, Philip Scheltens, Jonathan M Schott, Sudha Seshadri, Daoud Sie, Rebecca Sims, Erik A Sistermans, Sandro Sorbi, John C Van Swieten, Betty Tijms, André G Uitterlinden, Pieter Jelle Visser, Michael Wagner, David Wallon, Li-San Wang, Julie Williams, Jennifer S Yokoyama, Aline Zarea, Sven J van der Lee, Johan G Olsen, Marc Hulsman, Henne Holstege Show less
Protein truncating variants (PTVs) in To identify high-priority missense variants (HPVs), we applied ‘domain mapping of disease mutations’ for the 637 unique coding In this sample, PTVs and HPVs assoc Show more
Protein truncating variants (PTVs) in To identify high-priority missense variants (HPVs), we applied ‘domain mapping of disease mutations’ for the 637 unique coding In this sample, PTVs and HPVs associated with respectively a 35- and 10-fold increased risk of early onset AD and 17- and 6-fold increased risk of overall AD. The median age at onset (AAO) of PTV- and HPV-carriers was 62 and 64 years, and Our results justify a debate on whether HPV carriers should be considered for clinical counseling. The online version contains supplementary material available at 10.1186/s13024-025-00907-z. Show less
📄 PDF DOI: 10.1186/s13024-025-00907-z
APOE
G Jun, C A Ibrahim-Verbaas, M Vronskaya +115 more · 2016 · Molecular psychiatry · Nature · added 2026-04-24
APOE ɛ4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics o Show more
APOE ɛ4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics of Alzheimer's Project (IGAP) Consortium in APOE ɛ4+ (10 352 cases and 9207 controls) and APOE ɛ4- (7184 cases and 26 968 controls) subgroups as well as in the total sample testing for interaction between a single-nucleotide polymorphism (SNP) and APOE ɛ4 status. Suggestive associations (P<1 × 10(-4)) in stage 1 were evaluated in an independent sample (stage 2) containing 4203 subjects (APOE ɛ4+: 1250 cases and 536 controls; APOE ɛ4-: 718 cases and 1699 controls). Among APOE ɛ4- subjects, novel genome-wide significant (GWS) association was observed with 17 SNPs (all between KANSL1 and LRRC37A on chromosome 17 near MAPT) in a meta-analysis of the stage 1 and stage 2 data sets (best SNP, rs2732703, P=5·8 × 10(-9)). Conditional analysis revealed that rs2732703 accounted for association signals in the entire 100-kilobase region that includes MAPT. Except for previously identified AD loci showing stronger association in APOE ɛ4+ subjects (CR1 and CLU) or APOE ɛ4- subjects (MS4A6A/MS4A4A/MS4A6E), no other SNPs were significantly associated with AD in a specific APOE genotype subgroup. In addition, the finding in the stage 1 sample that AD risk is significantly influenced by the interaction of APOE with rs1595014 in TMEM106B (P=1·6 × 10(-7)) is noteworthy, because TMEM106B variants have previously been associated with risk of frontotemporal dementia. Expression quantitative trait locus analysis revealed that rs113986870, one of the GWS SNPs near rs2732703, is significantly associated with four KANSL1 probes that target transcription of the first translated exon and an untranslated exon in hippocampus (P ⩽ 1.3 × 10(-8)), frontal cortex (P ⩽ 1.3 × 10(-9)) and temporal cortex (P⩽1.2 × 10(-11)). Rs113986870 is also strongly associated with a MAPT probe that targets transcription of alternatively spliced exon 3 in frontal cortex (P=9.2 × 10(-6)) and temporal cortex (P=2.6 × 10(-6)). Our APOE-stratified GWAS is the first to show GWS association for AD with SNPs in the chromosome 17q21.31 region. Replication of this finding in independent samples is needed to verify that SNPs in this region have significantly stronger effects on AD risk in persons lacking APOE ɛ4 compared with persons carrying this allele, and if this is found to hold, further examination of this region and studies aimed at deciphering the mechanism(s) are warranted. Show less
📄 PDF DOI: 10.1038/mp.2015.23
KANSL1
G Davies, N Armstrong, J C Bis +126 more · 2015 · Molecular psychiatry · Nature · added 2026-04-24
G Davies, N Armstrong, J C Bis, J Bressler, V Chouraki, S Giddaluru, E Hofer, C A Ibrahim-Verbaas, M Kirin, J Lahti, S J van der Lee, S Le Hellard, T Liu, R E Marioni, C Oldmeadow, I Postmus, A V Smith, J A Smith, A Thalamuthu, R Thomson, V Vitart, J Wang, L Yu, L Zgaga, W Zhao, R Boxall, S E Harris, W D Hill, D C Liewald, M Luciano, H Adams, D Ames, N Amin, P Amouyel, A A Assareh, R Au, J T Becker, A Beiser, C Berr, L Bertram, E Boerwinkle, B M Buckley, H Campbell, J Corley, P L De Jager, C Dufouil, J G Eriksson, T Espeseth, J D Faul, I Ford, Generation Scotland, R F Gottesman, M E Griswold, V Gudnason, T B Harris, G Heiss, A Hofman, E G Holliday, J Huffman, S L R Kardia, N Kochan, D S Knopman, J B Kwok, J-C Lambert, T Lee, G Li, S-C Li, M Loitfelder, O L Lopez, A J Lundervold, A Lundqvist, K A Mather, S S Mirza, L Nyberg, B A Oostra, A Palotie, G Papenberg, A Pattie, K Petrovic, O Polasek, B M Psaty, P Redmond, S Reppermund, J I Rotter, H Schmidt, M Schuur, P W Schofield, R J Scott, V M Steen, D J Stott, J C van Swieten, K D Taylor, J Trollor, S Trompet, A G Uitterlinden, G Weinstein, E Widen, B G Windham, J W Jukema, A F Wright, M J Wright, Q Yang, H Amieva, J R Attia, D A Bennett, H Brodaty, A J M de Craen, C Hayward, M A Ikram, U Lindenberger, L-G Nilsson, D J Porteous, K Räikkönen, I Reinvang, I Rudan, P S Sachdev, R Schmidt, P R Schofield, V Srikanth, J M Starr, S T Turner, D R Weir, J F Wilson, C van Duijn, L Launer, A L Fitzpatrick, S Seshadri, T H Mosley, I J Deary Show less
General cognitive function is substantially heritable across the human life course from adolescence to old age. We investigated the genetic contribution to variation in this important, health- and wel Show more
General cognitive function is substantially heritable across the human life course from adolescence to old age. We investigated the genetic contribution to variation in this important, health- and well-being-related trait in middle-aged and older adults. We conducted a meta-analysis of genome-wide association studies of 31 cohorts (N=53,949) in which the participants had undertaken multiple, diverse cognitive tests. A general cognitive function phenotype was tested for, and created in each cohort by principal component analysis. We report 13 genome-wide significant single-nucleotide polymorphism (SNP) associations in three genomic regions, 6q16.1, 14q12 and 19q13.32 (best SNP and closest gene, respectively: rs10457441, P=3.93 × 10(-9), MIR2113; rs17522122, P=2.55 × 10(-8), AKAP6; rs10119, P=5.67 × 10(-9), APOE/TOMM40). We report one gene-based significant association with the HMGN1 gene located on chromosome 21 (P=1 × 10(-6)). These genes have previously been associated with neuropsychiatric phenotypes. Meta-analysis results are consistent with a polygenic model of inheritance. To estimate SNP-based heritability, the genome-wide complex trait analysis procedure was applied to two large cohorts, the Atherosclerosis Risk in Communities Study (N=6617) and the Health and Retirement Study (N=5976). The proportion of phenotypic variation accounted for by all genotyped common SNPs was 29% (s.e.=5%) and 28% (s.e.=7%), respectively. Using polygenic prediction analysis, ~1.2% of the variance in general cognitive function was predicted in the Generation Scotland cohort (N=5487; P=1.5 × 10(-17)). In hypothesis-driven tests, there was significant association between general cognitive function and four genes previously associated with Alzheimer's disease: TOMM40, APOE, ABCG1 and MEF2C. Show less
📄 PDF DOI: 10.1038/mp.2014.188
AKAP6
Marie-Laure Ancelin, Emmanuelle Ripoche, Anne-Marie Dupuy +6 more · 2013 · Journal of Alzheimer's disease : JAD · added 2026-04-24
Cholesterol is a risk factor for developing vascular pathologies, which is in turn an important risk factor for dementia. Previous studies linking lipids and dementia have yielded inconsistent results Show more
Cholesterol is a risk factor for developing vascular pathologies, which is in turn an important risk factor for dementia. Previous studies linking lipids and dementia have yielded inconsistent results, which may be attributable to sex differences in the etiology of both vascular disease and dementia. The aim of this study was to evaluate the associations between lipids and incident dementia in 7053 community-dwelling elderly. Dementia was diagnosed at baseline, and 2, 4, and 7-year follow-up. Multivariate Cox models stratified by sex and history of vascular pathologies at baseline were adjusted for sociodemographic, mental and physical health variables, and genetic vulnerability. In men without vascular pathologies, an increased incidence of all-cause dementia but not Alzheimer's disease (AD) was associated with high triglyceride (TG) (HR = 1.55, 95% CI = 1.04-2.32, p = 0.03) and low HDL-cholesterol levels (HR = 1.49, 95% CI = 0.99-2.23, p = 0.05). In women without vascular pathologies, low TG levels were associated with a decreased risk of AD (HR = 0.65, 95% CI = 0.43-0.97, p = 0.03). A decreased risk was also found with high TG levels which may depend on genetic vulnerability to dyslipidemia related to APOA5. For both sexes, no significant associations were found between total- or LDL-cholesterol and dementia or AD. Low HDL-cholesterol and high TG levels may be risk factors of dementia in elderly men whereas low TG is associated with decreased incident AD in women. This data suggests a complex sex-specific etiology of vascular dementia and AD. Show less
no PDF DOI: 10.3233/JAD-121228
APOA5