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Methylomic profiling implicates cortical deregulation of ANK1 in Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is a chronic neurodegenerative disorder that is characterized by progressive neuropathology and cognitive decline. We performed a cross-tissue analysis of methylomic variation in AD using samples from four independent human post-mortem brain cohorts. We identified a differentially methylated region in the ankyrin 1 (ANK1) gene that was associated with neuropathology in the entorhinal cortex, a primary site of AD manifestation. This region was confirmed as being substantially hypermethylated in two other cortical regions (superior temporal gyrus and prefrontal cortex), but not in the cerebellum, a region largely protected from neurodegeneration in AD, or whole blood obtained pre-mortem from the same individuals. Neuropathology-associated ANK1 hypermethylation was subsequently confirmed in cortical samples from three independent brain cohorts. This study represents, to the best of our knowledge, the first epigenome-wide association study of AD employing a sequential replication design across multiple tissues and highlights the power of this approach for identifying methylomic variation associated with complex disease.
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“Importantly, alterations of DNA methylation levels have also been implicated in multiple neurological disorders including AD [18–22]”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [19]
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“Consistent with previous studies [18, 19, 86, 87], we observed the majority of these sex-specific differences were hyper-methylated in samples with AD neuropathology, for which methylation levels increased as the AD Braak stage increased”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [19]
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“Alterations of DNA methylation levels have been shown to be involved in many diseases, including AD [19–24].”
From Distinct sex-specific DNA methylation differences in Alzheimer’s disease (2022) · cites this paper as [20]
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“consistent with previous studies in AD that also found DNA methylation variations in the blood, by and large, did not recapitulate those in the brain [20, 22, 93].”
From Distinct sex-specific DNA methylation differences in Alzheimer’s disease (2022) · cites this paper as [20]
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“DNA methylation is an important epigenetic modification that regulates gene transcription and is known to be involved in AD”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [19]
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“Notably, none of the 14 CpGs detected in our interaction analysis was identified in previous large-scale DNA methylation studies [18–22]”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [19]
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“and two independent genome-wide studies recently identified a differentially methylated region in the ANK1 gene as associated with the burden of AD pathology [198, 199].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [198]
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Metadata
- Authors
- Lunnon, K., Smith, R., Hannon, E., De Jager, P. L., Srivastava, G., Volta, M., Troakes, C., Al-Sarraj, S., Burrage, J., Macdonald, R., Condliffe, D., Harries, L. W., Katsel, P., Haroutunian, V., Kaminsky, Z., Joachim, C., Powell, J., Lovestone, S., Bennett, D. A., Schalkwyk, L. C., & Mill, J.
- Affiliations
- University of Exeter (GB)
- King's College London (GB)
- Broad Institute (US)
- Icahn School of Medicine at Mount Sinai (US)
- Johns Hopkins University (US)
- John Radcliffe Hospital (GB)
- Rush University Medical Center (US)
- Corresponding author
- Mill, Jonathan
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2014-08-17
- Volume
- 17
- Issue
- 9
- Pages
- 1164-1170
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4410018
- OpenAlex
- W1991244004
- Cited by
- 574
- References
- 47
- Citations by year
- 2026: 26 · 2025: 38 · 2024: 43 · 2023: 46 · 2022: 49 · 2021: 56 · 2020: 65 · 2019: 46 · 2018: 56 · 2017: 41 · 2016: 56 · 2015: 37 · 2014: 15
- FWCI
- 20.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Open Access at Essex (University of Essex) (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Figshare (submittedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Open Research Exeter (University of Exeter) (submittedVersion)
- Funders
- Medical Research Council (MR/L022656/1)
- National Institute on Aging (R01AG017917, P30-AG 10161, K25AG041906, R01AG036039, AG-02219, R01‐AG17917, R01 AG15819, R01AG018023, R01AG036836, AG 05138, P50AG005138, R01-AG18023, R01AG036042, R01AG015819, P30AG010161, RC2AG036547, R01AG032990, P01AG002219, RF1AG036042, P50AG016574)
- National Institute of Mental Health (R01MH064673, MH-064673)
- National Institute of Environmental Health Sciences (U01ES017155)
- National Center for Research Resources (KL2RR024151)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, ANK1, DNA methylation, hypermethylation, differentially methylated regions, entorhinal cortex, superior temporal gyrus, prefrontal cortex, cerebellum, epigenome-wide association study, postmortem brain
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Cerebral Cortex, Female, Humans, Male, Middle Aged, Temporal Lobe, Prefrontal Cortex, Ankyrins, Entorhinal Cortex, DNA Methylation, Epigenesis, Genetic, Genome-Wide Association Study, Transcriptome
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