ArticleNeurobiology of aging2020
APOE region molecular signatures of Alzheimer's disease across races/ethnicities.
Article in Neurobiology of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Interaction Analysis Reveals Complex Genetic Associations with Alzheimer's Disease in theGenes · 2023Pooled it
- Complex genetic interactions affect susceptibility to Alzheimer's disease risk in the BIN1 and MS4A6A loci.GeroScience · 2025Article
- Article
- The transition from genomics to phenomics in personalized population health.Nature reviews. Genetics · 2024Review
- Hormone replacement therapy, menopausal age and lifestyle variables are associated with better cognitive performance at follow-up but not cognition over time in older-adult women irrespective of APOE4 carrier status and co-morbidities.Frontiers in dementia · 2024Article
- Comparison of genetic and health risk factors for mild cognitive impairment and Alzheimer's disease between Hispanic and non-Hispanic white participants.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Neuropathology-based APOE genetic risk score better quantifies Alzheimer's risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Inter- and intra-chromosomal modulators of the APOE ɛ2 and ɛ4 effects on the Alzheimer's disease risk.GeroScience · 2023Article
- APOE ɛ4 allele and TOMM40-APOC1 variants jointly contribute to survival to older ages.Aging cell · 2022Article
- Genome-wide analysis identified abundant genetic modulators of contributions of the apolipoprotein E alleles to Alzheimer's disease risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Article
- Cerebrospinal Fluid Sphingomyelins in Alzheimer's Disease, Neurodegeneration, and Neuroinflammation.Journal of Alzheimer's disease : JAD · 2022Article
- Genetic Effects of NDUFAF6 rs6982393 and APOE on Alzheimer's Disease in Chinese Rural Elderly: A Cross-Sectional Population-Based Study.Clinical interventions in aging · 2022Article
- The APOE gene cluster responds to air pollution factors in mice with coordinated expression of genes that differs by age in humans.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- The ApoE Locus and COVID-19: Are We Going Where We Have Been?The journals of gerontology. Series A, Biological sciences and medical sciences · 2021Article
- Haplotype architecture of the Alzheimer's risk in theAlzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Review
- Expanding the scope of health disparities research in Alzheimer's disease and related dementias: Recommendations from the "Leveraging Existing Data and Analytic Methods for Health Disparities Research Related to Aging and Alzheimer's Disease and Related Dementias" Workshop Series.Alzheimer's & dementia (Amsterdam, Netherlands)Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The role of even the strongest genetic risk factor for Alzheimer's disease (AD), the apolipoprotein E (APOE) ε4 allele, in its etiology remains poorly understood. We examined molecular signatures of AD defined as differences in linkage disequilibrium patterns between AD-affected and -unaffected whites (2673/16,246), Hispanics (392/867), and African Americans (285/1789), separately. We focused on 29 polymorphisms from 5 genes in the APOE region emphasizing beneficial and adverse effects of the APOE ε2- and ε4-coding single-nucleotide polymorphisms, respectively, and the differences in the linkage disequilibrium structures involving these alleles between AD-affected and -unaffected subjects. Susceptibility to AD is likely the result of complex interactions of the ε2 and ε4 alleles with other polymorphisms in the APOE region, and these interactions differ across races/ethnicities corroborating differences in the adverse and beneficial effects of the ε4 and ε2 alleles. Our findings support complex race/ethnicity-specific haplotypes promoting and protecting against AD in this region. They contribute to better understanding of polygenic and resilient mechanisms, which can explain why even homozygous ε4 carriers may not develop AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.