A Multi-Center Study of ACE and the Risk of Late-Onset Alzheimer's Disease
Open accessAbstract
A key pathological feature of late-onset Alzheimer's disease (LOAD) is the abnormal extracellular accumulation of the amyloid-β (Aβ) peptide. Thus, altered Aβ degradation could be a major contributor to the development of LOAD. Variants in the gene encoding the Aβ-degrading enzyme, angiotensin-1 converting enzyme (ACE) therefore represent plausible candidates for association with LOAD pathology and risk. Following Alzgene meta-analyses of all published case-control studies, the ACE variants rs4291 and rs1800764 showed significant association with LOAD risk. Furthermore ACE haplotypes are associated with both plasma ACE levels and LOAD risk. We tested three ACE variants (rs4291, rs4343, and rs1800764) for association with LOAD in ten Caucasian case-control populations (n = 8,212). No association was found using multiple logistic models (all p > 0.09). We found no population heterogeneity (all p > 0.38) or evidence for association with LOAD risk following meta-analysis of the ten populations for rs4343 (OR = 1.00), rs4291 (OR = 0.97), or rs1800764 (OR = 0.99). Although we found no haplotypic association in our complete dataset (p = 0.51), a significant global haplotypic p-value was observed in one population (p = 0.007) due to an association of the H3 haplotype (OR = 0.72, p = 0.02) and a trend towards an association of H4 (OR = 1.38, p = 0.09) and H7 (OR = 2.07, p = 0.08) although these did not survive Bonferroni correction. Previously reported associations of ACE variants with LOAD will be diminished following this study. At best, ACE variants have modest effect sizes, which are likely part of a complex interaction between genetic, phenotypic and pharmacological effects that would be undetected in traditional case-control studies.
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ACE and ADAM10 were previously reported as Alzheimer's disease candidate genes but were not replicated in some subsequent studies.
“ACE and ADAM10 were previously reported as Alzheimer’s disease candidate genes18–22 but were not replicated in some subsequent studies23–25.”
From Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing (2019) · cites this paper as [25]
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- Authors
- Belbin, O., Brown, K., Shi, H., Medway, C., Abraham, R., Passmore, P., Mann, D., Smith, A. D., Holmes, C., McGuinness, B., Craig, D., Warden, D., Heun, R., Kölsch, H., Love, S., Kalsheker, N., Williams, J., Owen, M. J., Carrasquillo, M., Younkin, S., Morgan, K., & Kehoe, P. G.
- Affiliations
- University of Nottingham (GB)
- Cardiff University (GB)
- Queen's University Belfast (GB)
- University of Manchester (GB)
- University of Southampton (GB)
- University of Oxford (GB)
- Queen Elizabeth Hospital Birmingham (GB)
- University of Bonn (DE)
- Frenchay Hospital (GB)
- Mayo Clinic (US)
- Corresponding author
- Morgan, Kevin
- ORCID
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2011-05-10
- Volume
- 24
- Issue
- 3
- Pages
- 587-597
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC3655234
- OpenAlex
- W1697077861
- Cited by
- 34
- References
- 51
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 6 · 2013: 2 · 2012: 5
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Alzheimer s Disease (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Funders
- National Institute on Aging (U01 AG 06576, P50‐AG16574, AG03949, R01AG018023, U01AG006786, P01AG003949, AG 25711, R01-AG18023, AG 17216, U24 AG21886, P50AG025711, P01AG017216, U24AG021886, P50AG016574)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- angiotensin-converting enzyme, late-onset Alzheimer's disease
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Europe, Female, Gene Frequency, Genotype, Humans, Peptidyl-Dipeptidase A, Male, North America, Risk Factors, Meta-Analysis as Topic, Logistic Models, Odds Ratio, Case-Control Studies, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, White People
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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