Alzheimer's disease: early alterations in brain DNA methylation at ANK1, BIN1, RHBDF2 and other loci

Aging can lead to cognitive decline associated with neural pathology and Alzheimer's disease (AD). Here the authors scan the methylation status of CpGs across the entire genome of brain samples from aged subjects in an epigenome-wide association study (EWAS). Several loci, including ANK1, were...

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Published inNature neuroscience Vol. 17; no. 9; pp. 1156 - 1163
Main Authors De Jager, Philip L, Srivastava, Gyan, Lunnon, Katie, Burgess, Jeremy, Schalkwyk, Leonard C, Yu, Lei, Eaton, Matthew L, Keenan, Brendan T, Ernst, Jason, McCabe, Cristin, Tang, Anna, Raj, Towfique, Replogle, Joseph, Brodeur, Wendy, Gabriel, Stacey, Chai, High S, Younkin, Curtis, Younkin, Steven G, Zou, Fanggeng, Szyf, Moshe, Epstein, Charles B, Schneider, Julie A, Bernstein, Bradley E, Meissner, Alex, Ertekin-Taner, Nilufer, Chibnik, Lori B, Kellis, Manolis, Mill, Jonathan, Bennett, David A
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.09.2014
Nature Publishing Group
Subjects
45
45/43
631/1647/2210/2213
631/208/177
631/378/1689/1283
Adaptor Proteins, Signal Transducing - genetics
Aged
Aged, 80 and over
Alzheimer Disease - epidemiology
Alzheimer Disease - genetics
Alzheimer Disease - pathology
Alzheimer's disease
Amyloidosis - epidemiology
Amyloidosis - genetics
Amyloidosis - pathology
Animal Genetics and Genomics
Ankyrins - genetics
Behavioral Sciences
Biological Techniques
Biomedicine
Brain
Brain - pathology
Brain - physiology
Brain research
Carrier Proteins - genetics
CpG Islands - genetics
Development and progression
DNA methylation
DNA Methylation - genetics
Female
Genes
Genetic aspects
Genetic engineering
Genetic Predisposition to Disease - epidemiology
Genetic Predisposition to Disease - genetics
Genetic research
Genetic susceptibility
Genetic testing
Genome-Wide Association Study
Genomes
Genomics
Humans
Intracellular Signaling Peptides and Proteins
Male
Methylation
Middle Aged
Neurobiology
Neurosciences
Nuclear Proteins - genetics
Pathology
Protein Interaction Maps
Tumor Suppressor Proteins - genetics
United Kingdom > UK
Florida
United States > US
Massachusetts
Online AccessGet full text

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Abstract Aging can lead to cognitive decline associated with neural pathology and Alzheimer's disease (AD). Here the authors scan the methylation status of CpGs across the entire genome of brain samples from aged subjects in an epigenome-wide association study (EWAS). Several loci, including ANK1, were associated with AD pathology, gene expression and AD genetic risk networks. We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). We found that the level of methylation at 71 of the 415,848 interrogated CpGs was significantly associated with the burden of AD pathology, including CpGs in the ABCA7 and BIN1 regions, which harbor known AD susceptibility variants. We validated 11 of the differentially methylated regions in an independent set of 117 subjects. Furthermore, we functionally validated these CpG associations and identified the nearby genes whose RNA expression was altered in AD: ANK1 , CDH23 , DIP2A , RHBDF2 , RPL13 , SERPINF1 and SERPINF2 . Our analyses suggest that these DNA methylation changes may have a role in the onset of AD given that we observed them in presymptomatic subjects and that six of the validated genes connect to a known AD susceptibility gene network.
AbstractList We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). We found that the level of methylation at 71 of the 415,848 interrogated CpGs was significantly associated with the burden of AD pathology, including CpGs in the ABCA7 and BIN1 regions, which harbor known AD susceptibility variants. We validated 11 of the differentially methylated regions in an independent set of 117 subjects. Furthermore, we functionally validated these CpG associations and identified the nearby genes whose RNA expression was altered in AD: ANK1, CDH23, DIP2A, RHBDF2, RPL13, SERPINF1 and SERPINF2. Our analyses suggest that these DNA methylation changes may have a role in the onset of AD given that we observed them in presymptomatic subjects and that six of the validated genes connect to a known AD susceptibility gene network.
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). We found that the level of methylation at 71 of the 415,848 interrogated CpGs was significantly associated with the burden of AD pathology, including CpGs in the ABCA7 and BIN1 regions, which harbor known AD susceptibility variants. We validated 11 of the differentially methylated regions in an independent set of 117 subjects. Furthermore, we functionally validated these CpG associations and identified the nearby genes whose RNA expression was altered in AD: ANK1, CDH23, DIP2A, RHBDF2, RPL13, SERPINF1 and SERPINF2. Our analyses suggest that these DNA methylation changes may have a role in the onset of AD given that we observed them in presymptomatic subjects and that six of the validated genes connect to a known AD susceptibility gene network.We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). We found that the level of methylation at 71 of the 415,848 interrogated CpGs was significantly associated with the burden of AD pathology, including CpGs in the ABCA7 and BIN1 regions, which harbor known AD susceptibility variants. We validated 11 of the differentially methylated regions in an independent set of 117 subjects. Furthermore, we functionally validated these CpG associations and identified the nearby genes whose RNA expression was altered in AD: ANK1, CDH23, DIP2A, RHBDF2, RPL13, SERPINF1 and SERPINF2. Our analyses suggest that these DNA methylation changes may have a role in the onset of AD given that we observed them in presymptomatic subjects and that six of the validated genes connect to a known AD susceptibility gene network.
Aging can lead to cognitive decline associated with neural pathology and Alzheimer's disease (AD). Here the authors scan the methylation status of CpGs across the entire genome of brain samples from aged subjects in an epigenome-wide association study (EWAS). Several loci, including ANK1, were associated with AD pathology, gene expression and AD genetic risk networks. We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). We found that the level of methylation at 71 of the 415,848 interrogated CpGs was significantly associated with the burden of AD pathology, including CpGs in the ABCA7 and BIN1 regions, which harbor known AD susceptibility variants. We validated 11 of the differentially methylated regions in an independent set of 117 subjects. Furthermore, we functionally validated these CpG associations and identified the nearby genes whose RNA expression was altered in AD: ANK1 , CDH23 , DIP2A , RHBDF2 , RPL13 , SERPINF1 and SERPINF2 . Our analyses suggest that these DNA methylation changes may have a role in the onset of AD given that we observed them in presymptomatic subjects and that six of the validated genes connect to a known AD susceptibility gene network.
Audience Academic
Author Keenan, Brendan T
Bernstein, Bradley E
Ertekin-Taner, Nilufer
Younkin, Steven G
Chai, High S
Schneider, Julie A
Lunnon, Katie
Eaton, Matthew L
Mill, Jonathan
Kellis, Manolis
Bennett, David A
Tang, Anna
Epstein, Charles B
De Jager, Philip L
McCabe, Cristin
Chibnik, Lori B
Meissner, Alex
Gabriel, Stacey
Yu, Lei
Raj, Towfique
Younkin, Curtis
Replogle, Joseph
Szyf, Moshe
Brodeur, Wendy
Schalkwyk, Leonard C
Srivastava, Gyan
Burgess, Jeremy
Zou, Fanggeng
Ernst, Jason
Author_xml – sequence: 1
  givenname: Philip L
  surname: De Jager
  fullname: De Jager, Philip L
  email: pdejager@partners.org
  organization: Departments of Neurology and Psychiatry, Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Brigham and Women's Hospital, Harvard Medical School, Program in Medical and Population Genetics, Broad Institute
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  givenname: Gyan
  surname: Srivastava
  fullname: Srivastava, Gyan
  organization: Departments of Neurology and Psychiatry, Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Brigham and Women's Hospital, Program in Medical and Population Genetics, Broad Institute
– sequence: 3
  givenname: Katie
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  fullname: Lunnon, Katie
  organization: University of Exeter Medical School, University of Exeter, Institute of Psychiatry, King's College London
– sequence: 4
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  surname: Burgess
  fullname: Burgess, Jeremy
  organization: Department of Neuroscience, Mayo Clinic, Department of Neurology, Mayo Clinic
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  orcidid: 0000-0001-7030-5756
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  givenname: Matthew L
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  givenname: Brendan T
  surname: Keenan
  fullname: Keenan, Brendan T
  organization: Departments of Neurology and Psychiatry, Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Brigham and Women's Hospital, Program in Medical and Population Genetics, Broad Institute
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  surname: Ernst
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  surname: Tang
  fullname: Tang, Anna
  organization: Departments of Neurology and Psychiatry, Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Brigham and Women's Hospital
– sequence: 12
  givenname: Towfique
  surname: Raj
  fullname: Raj, Towfique
  organization: Departments of Neurology and Psychiatry, Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Brigham and Women's Hospital, Harvard Medical School, Program in Medical and Population Genetics, Broad Institute
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  givenname: Joseph
  surname: Replogle
  fullname: Replogle, Joseph
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  surname: Brodeur
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  organization: Genetic Analysis Platform, Broad Institute
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  organization: Department of Neuroscience, Mayo Clinic, Department of Neurology, Mayo Clinic
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  organization: Department of Neuroscience, Mayo Clinic
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  organization: Department of Neuroscience, Mayo Clinic
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  organization: Epigenomics Program, Broad Institute
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  email: david_a_bennett@rush.edu
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25129075$$D View this record in MEDLINE/PubMed
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SSID ssj0007589
Score 2.6364179
Snippet Aging can lead to cognitive decline associated with neural pathology and Alzheimer's disease (AD). Here the authors scan the methylation status of CpGs across...
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease...
SourceID proquest
gale
pubmed
crossref
springer
SourceType Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 1156
SubjectTerms 45
45/43
631/1647/2210/2213
631/208/177
631/378/1689/1283
Adaptor Proteins, Signal Transducing - genetics
Aged
Aged, 80 and over
Alzheimer Disease - epidemiology
Alzheimer Disease - genetics
Alzheimer Disease - pathology
Alzheimer's disease
Amyloidosis - epidemiology
Amyloidosis - genetics
Amyloidosis - pathology
Animal Genetics and Genomics
Ankyrins - genetics
Behavioral Sciences
Biological Techniques
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Brain
Brain - pathology
Brain - physiology
Brain research
Carrier Proteins - genetics
CpG Islands - genetics
Development and progression
DNA methylation
DNA Methylation - genetics
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Genetic Predisposition to Disease - epidemiology
Genetic Predisposition to Disease - genetics
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Genome-Wide Association Study
Genomes
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Intracellular Signaling Peptides and Proteins
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Methylation
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Neurobiology
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Nuclear Proteins - genetics
Pathology
Protein Interaction Maps
Tumor Suppressor Proteins - genetics
Title Alzheimer's disease: early alterations in brain DNA methylation at ANK1, BIN1, RHBDF2 and other loci
URI https://link.springer.com/article/10.1038/nn.3786
https://www.ncbi.nlm.nih.gov/pubmed/25129075
https://www.proquest.com/docview/1656322933
https://www.proquest.com/docview/1558526781
https://www.proquest.com/docview/1664205157
Volume 17
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