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000139044 0247_ $$2doi$$a10.1038/mp.2016.18
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000139044 0247_ $$2ISSN$$a1476-5578
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000139044 037__ $$aDZNE-2020-05366
000139044 041__ $$aEnglish
000139044 082__ $$a610
000139044 1001_ $$0P:(DE-2719)2810305$$aLacour, Andre$$b0$$eFirst author$$udzne
000139044 245__ $$aGenome-wide significant risk factors for Alzheimer's disease: role in progression to dementia due to Alzheimer's disease among subjects with mild cognitive impairment.
000139044 260__ $$aLondon$$bMacmillan$$c2017
000139044 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2016-03-15
000139044 264_1 $$2Crossref$$3print$$bSpringer Science and Business Media LLC$$c2017-01-01
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000139044 520__ $$aFew data are available concerning the role of risk markers for Alzheimer's disease (AD) in progression to AD dementia among subjects with mild cognitive impairment (MCI). We therefore investigated the role of well-known AD-associated single-nucleotide polymorphism (SNP) in the progression from MCI to AD dementia. Four independent MCI data sets were included in the analysis: (a) the German study on Aging, Cognition and Dementia in primary care patients (n=853); (b) the German Dementia Competence Network (n=812); (c) the Fundació ACE from Barcelona, Spain (n=1245); and (d) the MCI data set of the Amsterdam Dementia Cohort (n=306). The effects of single markers and combined polygenic scores were measured using Cox proportional hazards models and meta-analyses. The clusterin (CLU) locus was an independent genetic risk factor for MCI to AD progression (CLU rs9331888: hazard ratio (HR)=1.187 (1.054-1.32); P=0.0035). A polygenic score (PGS1) comprising nine established genome-wide AD risk loci predicted a small effect on the risk of MCI to AD progression in APOE-ɛ4 (apolipoprotein E-ɛ4) carriers (HR=1.746 (1.029-2.965); P=0.038). The novel AD loci reported by the International Genomics of Alzheimer's Project were not implicated in MCI to AD dementia progression. SNP-based polygenic risk scores comprising currently available AD genetic markers did not predict MCI to AD progression. We conclude that SNPs in CLU are potential markers for MCI to AD progression.
000139044 536__ $$0G:(DE-HGF)POF3-344$$a344 - Clinical and Health Care Research (POF3-344)$$cPOF3-344$$fPOF III$$x0
000139044 536__ $$0G:(DE-HGF)POF3-345$$a345 - Population Studies and Genetics (POF3-345)$$cPOF3-345$$fPOF III$$x1
000139044 542__ $$2Crossref$$i2016-03-15$$uhttps://creativecommons.org/licenses/by-nc-nd/4.0
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000139044 650_7 $$2NLM Chemicals$$aApolipoprotein E4
000139044 650_7 $$2NLM Chemicals$$aBiomarkers
000139044 650_7 $$2NLM Chemicals$$aCLU protein, human
000139044 650_7 $$2NLM Chemicals$$aClusterin
000139044 650_2 $$2MeSH$$aAged
000139044 650_2 $$2MeSH$$aAged, 80 and over
000139044 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000139044 650_2 $$2MeSH$$aApolipoprotein E4: genetics
000139044 650_2 $$2MeSH$$aBiomarkers
000139044 650_2 $$2MeSH$$aClusterin: genetics
000139044 650_2 $$2MeSH$$aCognitive Dysfunction: genetics
000139044 650_2 $$2MeSH$$aDementia: genetics
000139044 650_2 $$2MeSH$$aDisease Progression
000139044 650_2 $$2MeSH$$aFemale
000139044 650_2 $$2MeSH$$aFollow-Up Studies
000139044 650_2 $$2MeSH$$aGenetic Predisposition to Disease
000139044 650_2 $$2MeSH$$aGenome-Wide Association Study: methods
000139044 650_2 $$2MeSH$$aHumans
000139044 650_2 $$2MeSH$$aMale
000139044 650_2 $$2MeSH$$aMiddle Aged
000139044 650_2 $$2MeSH$$aPolymorphism, Single Nucleotide: genetics
000139044 650_2 $$2MeSH$$aRisk Factors
000139044 7001_ $$aEspinosa, A.$$b1
000139044 7001_ $$aLouwersheimer, E.$$b2
000139044 7001_ $$aHeilmann, S.$$b3
000139044 7001_ $$0P:(DE-HGF)0$$aHernández, I.$$b4
000139044 7001_ $$0P:(DE-2719)2810544$$aWolfsgruber, S.$$b5$$udzne
000139044 7001_ $$aFernández, V.$$b6
000139044 7001_ $$0P:(DE-2719)2000057$$aWagner, H.$$b7$$udzne
000139044 7001_ $$aRosende-Roca, M.$$b8
000139044 7001_ $$aMauleón, A.$$b9
000139044 7001_ $$aMoreno-Grau, S.$$b10
000139044 7001_ $$aVargas, L.$$b11
000139044 7001_ $$aPijnenburg, Y. A. L.$$b12
000139044 7001_ $$aKoene, T.$$b13
000139044 7001_ $$aRodríguez-Gómez, O.$$b14
000139044 7001_ $$aOrtega, G.$$b15
000139044 7001_ $$aRuiz, S.$$b16
000139044 7001_ $$aHolstege, H.$$b17
000139044 7001_ $$aSotolongo-Grau, O.$$b18
000139044 7001_ $$aKornhuber, J.$$b19
000139044 7001_ $$0P:(DE-HGF)0$$aPeters, O.$$b20
000139044 7001_ $$aFrölich, L.$$b21
000139044 7001_ $$aHüll, M.$$b22
000139044 7001_ $$0P:(DE-HGF)0$$aRüther, E.$$b23
000139044 7001_ $$0P:(DE-HGF)0$$aWiltfang, J.$$b24
000139044 7001_ $$aScherer, M.$$b25
000139044 7001_ $$aRiedel-Heller, S.$$b26
000139044 7001_ $$aAlegret, M.$$b27
000139044 7001_ $$0P:(DE-HGF)0$$aNöthen, M. M.$$b28
000139044 7001_ $$aScheltens, P.$$b29
000139044 7001_ $$aTárraga, L.$$b30
000139044 7001_ $$0P:(DE-2719)2000032$$aJessen, F.$$b31$$udzne
000139044 7001_ $$aBoada, M.$$b32
000139044 7001_ $$0P:(DE-2719)2000015$$aMaier, W.$$b33$$udzne
000139044 7001_ $$avan der Flier, W. M.$$b34
000139044 7001_ $$0P:(DE-2719)2501867$$aBecker, T.$$b35$$udzne
000139044 7001_ $$0P:(DE-HGF)0$$aRamirez, A.$$b36
000139044 7001_ $$0P:(DE-HGF)0$$aRuiz, A.$$b37$$eCorresponding author
000139044 77318 $$2Crossref$$3journal-article$$a10.1038/mp.2016.18$$b : Springer Science and Business Media LLC, 2016-03-15$$n1$$p153-160$$tMolecular Psychiatry$$v22$$x1359-4184$$y2016
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000139044 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5414086
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