4 research outputs found
New insights into the genetic etiology of Alzheimer's disease and related dementias
- Author
- Aaltonen L.
- Aaltonen V.
- Aarsland Dag
- Aavikko M.
- Abalos M.S.
- Abdelnour Carla
- Abner E.
- Abraham R.
- Adams H.
- Adams P.M.
- Adarmes-GĂłmez A.
- Adarmes-GĂłmez A.D.
- Aguilera N.
- Aguilera N.
- Aguirre A.
- Ahmad S.
- Akinyemi R.O.
- Al-Chalabi A.
- AlarcĂłn-MartĂn Emilio
- Albert M.S.
- Albin R.L.
- Alcolea Daniel
- Alegret Montserrat
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- Allende I.R.
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- Publication date
- 01/01/2022
- Field of study
Get PDFCharacterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele
Generalized Skeletal Abnormalities
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- A. Coin
- A. Kirchgatterer
- A. Superti-Furga
- A.E. Rosenberg
- A.G. Uitterlinden
- A.G.W. Hunter
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- F.W. Lafferty
- G. Jones
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- H.K. Genant
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- H.P. Chase
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- W. Dihlmann
- W.H. Akeson
- W.M. Clouston
- Y. Gong
- Y. Gong
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2005
- Field of study
No full textEvidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index
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- Adamo P. (Pio) d'
- Adan R. (R.)
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- Elburg A.A. (Annemarie) van
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- Esko T. (TÔnu)
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- Estivill X. (Xavier)
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- Farmer A.E. (Anne E)
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- Klump K.L. (K. L.)
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- Koeleman B.P.C. (Bobby P. C.)
- Koeleman B.P.C. (Bobby)
- Kolcic I. (Ivana)
- Koller D.L. (Daniel)
- Komaki G. (Gen)
- Koubek D. (Doris)
- Kowgier M. (Matthew)
- Kraft P. (Peter)
- Kutalik Z. (ZoltĂĄn)
- La Via M. (Maria)
- Lakka T.A. (Timo)
- Lange L.A. (Leslie)
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- Launer L.J. (Lenore)
- Laven J.S. (J. S.)
- Lawlor D.A. (D. A.)
- Lawlor D.A. (Debbie)
- Le Hellard S. (Stephanie)
- LehtimÀki T. (Terho)
- Levitan R.D. (Robert D)
- Levy D. (D.)
- Lewin A. (Alex)
- Lewis C.M. (Cathryn)
- Li D. (Dong)
- Li S. (S.)
- Lichtenstein P. (Paul)
- Lilenfeld L. (Lisa)
- Lin P. (P.)
- Lindi V. (Virpi)
- Lissowska J. (Jolanta)
- Liu J. (J.)
- Logan D.W. (Darren W)
- Loos R.J.F. (Ruth)
- Lord G. (Graham)
- Lundervold A.J. (Astri)
- Lunetta K.L. (Kathryn)
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- McCarthy M.I. (M. I.)
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- Melbye M. (Mads)
- Merl E. (Elisabeth)
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- Meurs J.B.J. (Joyce) van
- Middeldorp C.M. (Christel)
- Millwood I.Y. (Iona)
- Mitchell J. (James)
- Mohlke K.L. (Karen)
- Monteleone P. (Palmiero)
- Montgomery G.W. (G. W.)
- Mook-Kanamori D.O. (D. O.)
- Murabito J. (Joanne)
- Murray J.C. (Jeffrey)
- MĂ€nnik K. (Katrin)
- MĂŒller T.D.
- Nalls M.A. (Michael)
- Navarro P. (Pau)
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- Nelis M. (M.)
- Nengut S.-G. (Suna-Gumuscu)
- Ness A.R. (A. R.)
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- Nivard M. (Michel)
- Nohr C. (Christian)
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- O'Reilly P.F. (P. F.)
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- Schosser A. (Alexandra)
- Schreiber S. (Stefan)
- Scuteri A. (A.)
- Scuteri A. (Angelo)
- Sebert S. (S.)
- SegrĂš A.V. (Ayellet)
- Sheerin N. (Neil)
- Siitonen N. (Niina)
- Simpkin D. (Douglas)
- Slachtova L. (Lenka)
- Sladek R. (Rob)
- Slagboom P.E. (Eline)
- Slof-Opât Landt M.C.T. (Margarita C. T.)
- Slopien A. (Agnieszka)
- Smith A.V. (Albert)
- Smith A.V. (Davey)
- Smith A.V. (Davey)
- Soranzo N. (Nicole)
- Soranzo N. (Nicole)
- Southam L. (Lorraine)
- Sovio U. (Ulla)
- Spector T.D. (Timothy)
- Srinivasan S.R. (Sathanur)
- Steen V.M. (Vidar)
- Stephens J. (Jonathan)
- Stolk L. (Lisette)
- Strachan D.P. (David)
- Streeten E.A. (Elizabeth)
- Strengman E. (Eric)
- Strober M. (Michael)
- Sulem P. (Patrick)
- Sullivan P.F. (Patrick)
- Sunyer J. (J.)
- Sunyer J. (Jordi)
- Szatkiewicz J.P. (Jin P)
- Szeszenia-Dabrowska N. (Neonila)
- SĂžrensen T.I.A. (Thorkild)
- Taal H.R. (Rob)
- Tachmazidou I. (Ioanna)
- Taico C. (Chrysecolla)
- Tammesoo M.L. (M. L.)
- Tenconi E. (Elena)
- Teo Y.Y. (Y. Y.)
- Teo Y.Y. (Yik Ying)
- Thiering E. (Elisabeth)
- Thornton L.M. (Laura)
- Thorsteinsdottir U. (Unnur)
- Tiesler C. (C.)
- Tikkanen E. (Emmi)
- Timpson N.J. (Nicholas)
- Toniolo D. (Daniela)
- Tortorella A. (Alfonso)
- Tozzi F. (Federica)
- Trace S.E. (Sara E)
- Treasure J. (Janet)
- Tryggvadottir L. (Laufey)
- Tschop M. (Matthias)
- Tschöp M.H. (M. H.)
- Tsitsika A. (Artemis)
- Tsitsika A. (Artemis)
- Tyrer J. (J.)
- Tziouvas K. (Konstantinos)
- Uda M. (M.)
- Uitterlinden A.G. (André)
- Ulivi S. (Shelia)
- ValcĂĄrcel B. (Beatriz)
- van Dam R.M. (R. M.)
- Vannberg F.O. (Frederik O)
- Versini A. (Audrey)
- Visser J.A. (Jenny)
- Volckmar A.-L. (A. L.)
- Vollenweider P. (Peter)
- Waeber G. (GĂ©rard)
- Wagner G. (Gudrun)
- Wareham N.J. (Nick)
- Warrington M. (M.)
- Warrington N.M. (Nicole)
- Waterworth D. (Dawn)
- Weedon M.N. (Michael)
- White S.J. (Stefan)
- Whittaker P. (Pamela)
- Wichmann H.E. (Heinz Erich)
- Widen E.
- Widen E. (E.)
- Willemsen G.A.H.M. (Gonneke)
- Wilson J.F. (J. F.)
- Wingerden S. (Sophie) van
- Winkler T.W. (Thomas W.)
- Woodside D.B. (D Blake)
- Wright A.F. (Alan)
- Yaghootkar H. (H.)
- Yilmaz Z. (Zeynep)
- Young L. (L.)
- Zeggini E. (Eleftheria)
- Zerwas S. (Stephanie)
- Zgaga L. (L.)
- Zhai G. (G.)
- Zhao J.H. (J. H.)
- Zhuang W.V. (W. V.)
- Zipfel S. (S.)
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/02/2017
- Field of study
No full textThe maintenance of normal body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time. Prior to the onset of AN, premorbid body mass index (BMI) spans the entire range from underweight to obese. After recovery, patients have reduced rates of overweight and obesity. As such, loci involved in body weight regulation may also be relevant for AN and vice versa. Our primary analysis comprised a cross-trait analysis of the 1000 single-nucleotide polymorphisms (SNPs) with the lowest P-values in a genome-wide association meta-analysis (GWAMA) of AN (GCAN) for evidence of association in the largest published GWAMA for BMI (GIANT). Subsequently we performed sex-stratified analyses for these 1000 SNPs. Functional ex vivo studies on four genes ensued. Lastly, a look-up of GWAMA-derived BMI-related loci was performed in the AN GWAMA. We detected significant associations (P-values <5 Ă 10-5, Bonferroni-corrected P<0.05) for nine SNP alleles at three independent loci. Interestingly, all AN susceptibility alleles were consistently associated with increased BMI. None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2: CARF and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previously been associated with AN or obesity. Sex-stratified analyses revealed that the strongest BMI signal originated predominantly from females (chr. 10 rs1561589; Poverall: 2.47 Ă 10-06/Pfemales: 3.45 Ă 10-07/Pmales: 0.043). Functional ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fasting. Hypothalamic expression of Ctbp2 was increased in diet-induced obese (DIO) mice as compared with age-matched lean controls. We observed no evidence for associations for the look-up of BMI-related loci in the AN GWAMA. A cross-trait analysis of AN and BMI loci revealed variants at three chromosomal loci with potential joint impact. The chromosome 10 locus is particularly promising given that the association with obesity was primarily driven by females. In addition, the detected altered hypothalamic expression patterns of Ctbp2 and Nbeal1 as a result of fasting and DIO implicate these genes in weight regulation
New insights into the genetic etiology of Alzheimerâs disease and related dementias
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
No full textCharacterization of the genetic landscape of Alzheimerâs disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/âproxyâ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele. © 2022, The Author(s)
