APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimer’s Disease
Abstract
To the Editor: The report by Quiroz et al. (June 20 issue) 1 on the Colombian PSEN1 E280A pedigree suggests a protective effect of apolipoprotein E3 Christchurch ( APOE3 Ch ) variant heterozygosity. The signal from 27 carriers is driven by 13 carriers in whom mild cognitive impairment or dementia developed. A previous study assessed 11 of these 13 heterozygotes with the use of age-at-onset data systematically collected before knowledge of the APOE3 Ch variant; the median age at onset of mild cognitive impairment was 1 year earlier in APOE3 Ch carriers than in noncarriers, and the median age at onset of dementia was equal in carriers . . .
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The heterozygote finding has been contended.
“The heterozygote finding has been contended 8 , however”
From Association of Rare <i>APOE</i> Missense Variants R189C and W276C With Risk of Alzheimer Disease (2026) · cites this paper as [8]
Cites
Nelson, M. R., Liu, P., Agrawal, A., Yip, O., Blumenfeld, J., Traglia, M., Kim, M. J., Koutsodendris, N., Rao, A., Grone, B., et al. (2023) · Nature Neuroscience · doi:10.1038/s41593-023-01480-8 · Cited by 118 · see citing works
<i>APOE3</i> Christchurch Heterozygosity and Autosomal Dominant Alzheimer’s Disease
Quiroz, Y. T., Aguillon, D., Aguirre-Acevedo, D. C., Vasquez, D., Zuluaga, Y., Baena, A. Y., Madrigal, L., Hincapié, L., Sanchez, J. S., Langella, S., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2308583 · Cited by 63 · see citing works
Genetic associations with age at dementia onset in the <i>PSEN1 E280A</i> Colombian kindred
Cochran, J. N., Acosta‐Uribe, J., Esposito, B. T., Madrigal, L., Aguillón, D., Giraldo, M. M., Taylor, J. W., Bradley, J., Fulton‐Howard, B., Andrews, S. J., et al. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.13021 · Cited by 21 · see citing works
Self-citationNew insights into innate immunity in Alzheimer’s disease: From APOE protective variants to therapies
Chen, Y., & Holtzman, D. M. (2024) · Trends in Immunology · doi:10.1016/j.it.2024.08.001 · Cited by 19 · see citing works
Characterization of APOE Christchurch carriers in 455,306 UK Biobank participants
He, K. Y., Khramtsova, E. A., Cabrera-Socorro, A., Zhang, Y., Li, S., Sarver, B. A. J., Smets, B., Li, Q. S., De Muynck, L., Parrado, A. R., et al. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00684-7 · Cited by 8 · see citing works
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Association of Rare <i>APOE</i> Missense Variants R189C and W276C With Risk of Alzheimer Disease
Le Guen, Y., Reil, D., Jackson, R. J., Peña-Tauber, A., Khosla, C., & Greicius, M. D. (2026) · doi:10.64898/2026.05.08.26352778
Self-citationGenetic modifiers in autosomal dominant Alzheimer's disease
Kosik, K. S. (2026) · The Lancet Neurology · doi:10.1016/s1474-4422(26)00168-7
Toward personalized medicine in AD/ADRD through genetic-exposome dementia risk assessments
Tolosa‐Tort, P., Okorie, M., Chatterjee, A., Boeriu, A. I., Sharma, R. U., & Andrews, S. J. (2026) · npj Dementia · doi:10.1038/s44400-026-00087-7
- Authors
- Cochran, J. N., Greicius, M. D., & Goate, A.
- Affiliations
- HudsonAlpha Institute for Biotechnology (US)
- Stanford Medicine (US)
- Icahn School of Medicine at Mount Sinai (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2024-10-31
- Volume
- 391
- Issue
- 17
- Pages
- 1660-1661
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W4403912452
- Cited by
- 3
- References
- 5
- Citations by year
- 2026: 3
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- apolipoprotein E, autosomal dominant Alzheimer's disease, heterozygosity, age of onset, mild cognitive impairment, dementia, genetic risk
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