Genome-wide significant risk factors for Alzheimer’s disease: role in progression to dementia due to Alzheimer's disease among subjects with mild cognitive impairment

Few 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 t...

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Published inMolecular psychiatry Vol. 22; no. 1; pp. 153 - 160
Main Authors Lacour, A, Espinosa, A, Louwersheimer, E, Heilmann, S, Hernández, I, Wolfsgruber, S, Fernández, V, Wagner, H, Rosende-Roca, M, Mauleón, A, Moreno-Grau, S, Vargas, L, Pijnenburg, Y A L, Koene, T, Rodríguez-Gómez, O, Ortega, G, Ruiz, S, Holstege, H, Sotolongo-Grau, O, Kornhuber, J, Peters, O, Frölich, L, Hüll, M, Rüther, E, Wiltfang, J, Scherer, M, Riedel-Heller, S, Alegret, M, Nöthen, M M, Scheltens, P, Wagner, M, Tárraga, L, Jessen, F, Boada, M, Maier, W, van der Flier, W M, Becker, T, Ramirez, A, Ruiz, A
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.01.2017
Nature Publishing Group
Subjects
38/43
45/22
45/77
631/208
692/53
Aged
Aged, 80 and over
Alzheimer Disease - genetics
Apolipoprotein E4 - genetics
Behavioral Sciences
Biological Psychology
Biomarkers
Clusterin - genetics
Cognitive Dysfunction - genetics
Dementia
Dementia - genetics
Disease Progression
Female
Follow-Up Studies
Genetic Predisposition to Disease
Genome-Wide Association Study - methods
Humans
Male
Medicine
Medicine & Public Health
Middle Aged
Neurosciences
Original
original-article
Pharmacotherapy
Polymorphism, Single Nucleotide - genetics
Psychiatry
Risk Factors
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Abstract Few 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.
AbstractList Few 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 Fundacio 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- epsilon 4 (apolipoprotein E- epsilon 4) 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.
Few 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.
Few 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.
Few 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.
Few 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-[varepsilon]4 (apolipoprotein E-[varepsilon]4) 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.
Author Holstege, H
Vargas, L
Riedel-Heller, S
Rüther, E
van der Flier, W M
Frölich, L
Hüll, M
Pijnenburg, Y A L
Alegret, M
Lacour, A
Louwersheimer, E
Peters, O
Wiltfang, J
Rodríguez-Gómez, O
Fernández, V
Ruiz, A
Heilmann, S
Nöthen, M M
Tárraga, L
Ramirez, A
Mauleón, A
Jessen, F
Scherer, M
Rosende-Roca, M
Maier, W
Koene, T
Scheltens, P
Hernández, I
Ortega, G
Ruiz, S
Espinosa, A
Moreno-Grau, S
Sotolongo-Grau, O
Wagner, M
Becker, T
Kornhuber, J
Wagner, H
Wolfsgruber, S
Boada, M
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26976043$$D View this record in MEDLINE/PubMed
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Snippet Few data are available concerning the role of risk markers for Alzheimer’s disease (AD) in progression to AD dementia among subjects with mild cognitive...
Few data are available concerning the role of risk markers for Alzheimer's disease (AD) in progression to AD dementia among subjects with mild cognitive...
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pubmed
crossref
springer
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StartPage 153
SubjectTerms 38/43
45/22
45/77
631/208
692/53
Aged
Aged, 80 and over
Alzheimer Disease - genetics
Apolipoprotein E4 - genetics
Behavioral Sciences
Biological Psychology
Biomarkers
Clusterin - genetics
Cognitive Dysfunction - genetics
Dementia
Dementia - genetics
Disease Progression
Female
Follow-Up Studies
Genetic Predisposition to Disease
Genome-Wide Association Study - methods
Humans
Male
Medicine
Medicine & Public Health
Middle Aged
Neurosciences
Original
original-article
Pharmacotherapy
Polymorphism, Single Nucleotide - genetics
Psychiatry
Risk Factors
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Title Genome-wide significant risk factors for Alzheimer’s disease: role in progression to dementia due to Alzheimer's disease among subjects with mild cognitive impairment
URI https://link.springer.com/article/10.1038/mp.2016.18
https://www.ncbi.nlm.nih.gov/pubmed/26976043
https://www.proquest.com/docview/1850367978
https://www.proquest.com/docview/1859492515
https://pubmed.ncbi.nlm.nih.gov/PMC5414086
Volume 22
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