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Showing 10 of 382 rows for APOE genotype. One row per study per exposure: a study that tested two different things appears twice, once for each.
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| Exposure | Question | Direction | Outcome measured | Design | People | Effect size, as the source reported it | Source |
|---|---|---|---|---|---|---|---|
| APOE genotype Genes (not modifiable) | Prevention |
Mixed
whyDirection is for APOE genotype after 90: ε2 carriers had lower dementia risk, while the ε4 association was not statistically significant. Women and Black participants had higher risk than men and Asian participants. Age-standardised incidence was 116.82 per 1000 person-years. |
Incident all-cause dementia after age 90 by APOE genotype, sex and race | cohort study | 805 | The age-standardised incidence rate was 116·82 cases per 1000 person-years (95% CI 93·69-139·96). In Fine-Gray models, dementia risk was higher in female than in male participants (subdistribution hazard ratio [sHR] 1·89, 95% CI 1·30-2·76) and Black than Asian participants (sHR 1·75, 1·07-2·88), lower in APOE ε2 carriers than in non-carriers (sHR 0·39, 0·17-0·88), and not significantly higher in APOE ε4 carriers than in non-carriers (sHR 1·51, 0·92-2·47) |
The lancet. Healthy longevity
2026 ✓ Peer-reviewed PMID 42551464 |
| APOE genotype Genes (not modifiable) | Prevention |
Harm
whyDirection is for carrying APOE ε4: 10-year dementia risk ratios of 1.59 (Filipino, confidence interval crossing 1) to 1.96 (Japanese), similar across the four groups despite carrier prevalence ranging from 14% to 25%. Not modifiable. |
10-year dementia risk by APOE ε4 carriership in Chinese, Japanese, Filipino and non-Latino White adults | cohort study | 46,325 | 10-year risk ratios (95% confidence interval [CI]) ranged from 1.59 (0.66-3.10) among Filipino to 1.96 (1.36-2.78) among Japanese participants |
Alzheimer's & Dementia
2026 ✓ Peer-reviewed PMID 42427166 |
| APOE genotype Genes (not modifiable) | Prevention |
Harm
whyDirection is for each additional ε4 allele: it did not change amyloid-related p-tau217 secretion, but for any given p-tau217 level tau spread faster across connected regions, and the p-tau217 threshold marking early tau-PET increases was 26-76% lower than in non-carriers. |
Amyloid-associated plasma p-tau217 increase, and p-tau217-associated tau-PET spread, by APOE ε4 allele count | cohort study | 401 | plasma ptau217 elevations were linked to faster tau-PET spread from local epicentres across connected brain regions in an ApoE4 allele dose-dependent manner, independent of amyloid [ADNI/A4-LEARN: mean standardized beta (β) = 0.44/0.56, P < 0.001/P < 0.001] ... (ADNI: 0/1/2 ApoE4 alleles = 0.62/0.34/0.15 pg/ml, representing ∼45% and ∼76% reductions from non-carriers; Fujirebio ptau217 assay; A4-LEARN: 0/1/2 ApoE4 alleles = 0.31/0.23/0.18 pg/ml, representing ∼26% and ∼42% reductions; Eli Lilly ptau217 assay) |
Brain
2026 ✓ Peer-reviewed PMID 41410687 |
| APOE genotype Genes (not modifiable) | Prevention |
Benefit
whyDirection is for carrying the deletion, present in 60% of African American ε4 homozygotes: it reduced the AD odds ratio and delayed onset in ε4/ε4 cases with local African ancestry at APOE, confirmed in All of Us, and it abolishes SPI1 repression at the site. |
AD odds and age at onset in APOE ε4/ε4 carriers with versus without a 19 bp APOE enhancer deletion (African Americans) | case-control study | not stated | not established — the abstract states the deletion reduces the ad odds ratio and delays onset but prints no figure; only the 60% carrier frequency is given. |
Nature Communications
2026 ✓ Peer-reviewed PMID 41629326 |
| APOE genotype Genes (not modifiable) | Prevention |
No direction reported
whyA descriptive proteomic mapping: APOE-linked protein changes were present before amyloid pathology and stable across age and disease stage, with ε2 tied to cellular-maintenance and anti-inflammatory pathways and ε4 to cell-cycle, oligodendrocyte-precursor and downstream vascular, immune and proteostatic proteins. It estimates no effect on a clinical outcome. |
Plasma and CSF proteomic signatures of APOE ε4 and ε2 across five cohorts | cross-sectional study | not stated | not established — pubmed abstract reports no numeric effect size. |
Nature Aging
2026 ✓ Peer-reviewed PMID 42141098 |
| APOE genotype Genes (not modifiable) | Prevention |
Harm
whyDirection is for the APOE4 allele, whose effect ranged from OR 2.22 in Caribbean-Hispanic to 6.13 in Peruvian/Bolivian participants. The APOE2 allele went the other way (OR 0.81). Not modifiable. |
Alzheimer's disease and related dementias (odds ratio) | case-control study | 12,221 | APOE ε4 meta-analytic OR 2.32 (95% CI 2.09-2.57); range 2.22 (Caribbean-Hispanics) to 6.13 (Peruvians/Bolivians) |
Alzheimer's & Dementia
2025 ✓ Peer-reviewed PMID 40219824 |
| APOE genotype Genes (not modifiable) | Prevention |
Harm
whyDirection is for APOE ε4 carriage, which strengthened the association between amyloid and plasma p-tau; plasma GFAP strengthened the p-tau-tau PET link mainly in non-carriers, and high GFAP went with faster longitudinal tau accumulation. |
Strength of the amyloid-p-tau and p-tau-tau PET associations by APOE ε4 status and plasma GFAP, and longitudinal tau accumulation | cohort study | 806 | stronger Aβ–pTau associations observed in APOE ε4 carriers (CPAS: β = 0.26, p = 0.003 for pTau231; ADNI: β = 0.45, p < 0.001 for pTau181) |
Molecular Neurodegeneration
2025 ✓ Peer-reviewed PMID 41163175 |
| APOE genotype Genes (not modifiable) | Prevention |
Harm
whyDirection is for carrying two APOE4 copies: near-complete penetrance of Alzheimer's biology and earlier symptom onset. |
Alzheimer's biomarkers and age at symptom onset | cohort study | 10,039 | Nearly all APOE4 homozygotes showed Alzheimer's pathology by age 55 vs. about half of non-carriers |
Nature Medicine
2024 ✓ Peer-reviewed PMID 38710950 |
| APOE genotype Genes (not modifiable) | Prevention |
Harm
whyDirection is for carrying APOE*4: the ε3/ε4 odds ratio fell stepwise from 4.54 in East Asian to 3.46 in White, 2.18 in Black and 1.90 in Hispanic individuals; ε2 was protective in White and Black but not Hispanic or East Asian individuals. Not modifiable. |
Odds of Alzheimer's disease by APOE genotype, across ancestry, sex and age | case-control study | 68,756 | Odds ratios for APOE*34 and AD risk attenuated following East Asian (OR, 4.54; 95% CI, 3.99-5.17),White (OR, 3.46; 95% CI, 3.27-3.65), Black (OR, 2.18; 95% CI, 1.90-2.49) and Hispanic (OR, 1.90; 95% CI, 1.65-2.18) individuals. Similarly, ORs for APOE*22+23 and AD risk attenuated following White (OR, 0.53, 95% CI, 0.48-0.58), Black (OR, 0.69, 95% CI, 0.57-0.84), and Hispanic (OR, 0.89; 95% CI, 0.72-1.10) individuals |
JAMA Neurology
2023 ✓ Peer-reviewed PMID 37930705 |
| APOE genotype Genes (not modifiable) | Prevention |
Benefit
whyDirection is for carrying APOE2, which is associated with longer life irrespective of Alzheimer's status. The lifespan figures come from gene-targeted mice, not from the human cohort. |
Lifespan / survival | cohort study | 24,661 | Mice: "the median age at death was in the order of apoE2-TR (911 days) > apoE3 TR (825 days) > apoE4 TR (753 days) > Apoe KO (738 days)". In humans the abstract states only that "the association between APOE2 and longer lifespan persisted irrespective of AD status", without a numeric estimate. |
eLife
2020 ✓ Peer-reviewed PMID 33074098 |