ArticleAging cell2018
Apolipoprotein E region molecular signatures of Alzheimer's disease.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Interaction Analysis Reveals Complex Genetic Associations with Alzheimer's Disease in theGenes · 2023Pooled it
- Evaluation of the Genetic Variance of Alzheimer's Disease Explained by the Disease-Associated Chromosomal Regions.Journal of Alzheimer's disease : JAD · 2019Pooled it
- A novel method to disentangle tightly linked risk and resilience genes for brain disorders: application to Alzheimer's disease.Molecular psychiatry · 2026Article
- AI-Driven Transcriptome Prediction in Human Pathology: From Molecular Insights to Clinical Applications.Biology · 2025Review
- GWAS by Subtraction to Disentangle RBD Genetic Background from α-Synucleinopathies.International journal of molecular sciences · 2025Article
- Inter- and intra-chromosomal modulators of the APOE ɛ2 and ɛ4 effects on the Alzheimer's disease risk.GeroScience · 2023Article
- 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
- Challenges at the APOE locus: a robust quality control approach for accurate APOE genotyping.Alzheimer's research & therapy · 2022Article
- Definitive roles of TOMM40-APOE-APOC1 variants in the Alzheimer's risk.Neurobiology of aging · 2022Article
- Article
- 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
- Association of Uncommon, Noncoding Variants in the APOE Region With Risk of Alzheimer Disease in Adults of European Ancestry.JAMA network open · 2020Article
- MAPT haplotype-stratified GWAS reveals differential association for AD risk variants.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- APOE region molecular signatures of Alzheimer's disease across races/ethnicities.Neurobiology of aging · 2020Article
- Genetic and regulatory architecture of Alzheimer's disease in theAlzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Haplotype architecture of the Alzheimer's risk in theAlzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- THE EXPOSOME IN HUMAN EVOLUTION: FROM DUST TO DIESEL.The Quarterly review of biology · 2019Article
- Apolipoprotein C1: Its Pleiotropic Effects in Lipid Metabolism and Beyond.International journal of molecular sciences · 2019Review
- Gain and loss events in the evolution of the apolipoprotein family in vertebrata.BMC evolutionary biology · 2019Article
- The Alzheimer's Disease Exposome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2019Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Although the APOE region is the strongest genetic risk factor for Alzheimer's diseases (ADs), its pathogenic role remains poorly understood. Elucidating genetic predisposition to ADs, a subset of age-related diseases characteristic for postreproductive period, is hampered by the undefined role of evolution in establishing molecular mechanisms of such diseases. This uncertainty is inevitable source of natural-selection-free genetic heterogeneity in predisposition to ADs. We performed first large-scale analysis of linkage disequilibrium (LD) structures characterized by 30 polymorphisms from five genes in the APOE 19q13.3 region (BCAM, NECTIN2, TOMM40, APOE, and APOC1) in 2,673 AD-affected and 16,246 unaffected individuals from five cohorts. Consistent with the undefined role of evolution in age-related diseases, we found that these structures, being highly heterogeneous, are significantly different in subjects with and without ADs. The pattern of the difference represents molecular signature of AD comprised of single nucleotide polymorphisms (SNPs) from all five genes in the APOE region. Significant differences in LD in subjects with and without ADs indicate SNPs from different genes likely involved in AD pathogenesis. Significant and highly heterogeneous molecular signatures of ADs provide unprecedented insight into complex polygenetic predisposition to ADs in the APOE region. These findings are more consistent with a complex haplotype than with a single genetic variant origin of ADs in this region.
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