Confirmation that familial clustering and age of onset in late onset Alzheimer's disease are determined at the apolipoprotein E locus
Abstract
We confirm that familial clustering in late onset Alzheimer's disease is associated with the zeta 4 allele of apolipoprotein E. This allele occurs in the great majority (82%) of late onset familial Alzheimer cases. Together with previously published data, it is suggested that the effect of a single zeta 4 allele is to increase the risk of developing AD by an amount equivalent to 5 years and that the effect of zeta 4 homozygosity is to increase the risk of developing AD by an amount equivalent to 10 years of age.
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APOEε4 modifies the age at onset in both EOAD and LOAD.
“APOEε4 has been shown to modify the age at onset in both EOAD and LOAD [64–66].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [64]
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Apolipoprotein E polymorphism and atherosclerosis.
Davignon, J., Gregg, R. E., & Sing, C. F. (1988) · Arteriosclerosis: An Official Journal of the American Heart Association, Inc. · doi:10.1161/01.atv.8.1.1 · Cited by 1,981 · see citing works
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Apolipoprotein E, Dementia, and Cortical Deposition of β-Amyloid Protein
Polvikoski, T., Sulkava, R., Haltia, M., Kainulainen, K., Vuorio, A., Verkkoniemi, A., Niinistö, L., Halonen, P., & Kontula, K. (1995) · New England Journal of Medicine · doi:10.1056/nejm199511093331902 · Cited by 493 · see citing works
Genetic architecture of Alzheimer's disease
Neuner, S. M., TCW, J., & Goate, A. M. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.104976 · Cited by 126 · see citing works
“Given the overlap between EOAD and LOAD as discussed above, these modifiers may provide potential therapeutic targets for a more general population.”
Influential
- Authors
- Houlden, H., Crook, R., Hardy, J., Roques, P., Collinge, J., & Rossor, M.
- Affiliations
- University of South Florida (US)
- St Mary's Hospital (GB)
- Corresponding author
- Houlden, Henry
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1994-06
- Volume
- 174
- Issue
- 2
- Pages
- 222-224
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W1996623888
- Cited by
- 38
- References
- 1
- Citations by year
- 2025: 1 · 2020: 2 · 2019: 1 · 2015: 1 · 2012: 1
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institute on Aging (NIA-RO1 AG11871-01)
- 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
- late-onset Alzheimer's disease, apolipoprotein E, familial aggregation, age of onset, genetic risk, homozygosity
- MeSH terms
- Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Family, Genotype, Humans, Middle Aged, Age of Onset, Risk Assessment
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