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One row per finding: what was tested, which way the result went, and how the study was built. The answer by area, and where the studies disagree, are on the main page.
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Showing 4 of 382 rows. 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 |
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 |
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 |
| Rare protective or risk variant (APOE3 Christchurch, APOE R145C, RELN, FN1) Genes (not modifiable) | Prevention |
Benefit
whyDirection is for one copy of the APOE3 Christchurch variant: median onset of cognitive impairment at 52 versus 47 years in matched PSEN1 E280A carriers without it, with preserved brain metabolism and fewer vascular amyloid features in the few imaged or autopsied. Not modifiable. |
Age at onset of cognitive impairment in PSEN1 E280A carriers | cohort study | 1,077 | the median age at the onset of cognitive impairment was 52 years (95% confidence interval [CI], 51 to 58), in contrast to a matched group of PSEN1 E280A carriers without the APOE3 Ch variant, among whom the median age at the onset was 47 years (95% CI, 47 to 49) |
New England Journal of Medicine
2024 ✓ Peer-reviewed PMID 38899694 |
| Rare protective or risk variant (APOE3 Christchurch, APOE R145C, RELN, FN1) Genes (not modifiable) | Prevention |
Benefit
whyDirection is for carrying the rare FN1 variant rs140926439 in APOE ε4 homozygotes: odds of AD 0.29 and onset delayed 3.37 years in the 7185-person validation cohort, with zebrafish work suggesting fibronectin loss of function reduces gliosis. Not modifiable. |
Alzheimer's disease case status and age at onset among APOE ε4 homozygotes | case-control study | 7,185 | rs140926439 variant in FN1 was protective of AD (OR = 0.29; 95% CI [0.11, 0.78], P = 0.014) and delayed age at onset of disease by 3.37 years (95% CI [0.42, 6.32], P = 0.025) |
Acta Neuropathologica
2024 ✓ Peer-reviewed PMID 38598053 |