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Home › Research › What the research found › Every row

Every row of the evidence table

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.

Every row

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Area All 382 Care, carers and services 140 Medicines 85 Genes (not modifiable) 35 All modifiable factors together 27 Diet and supplements 23 Exercise and activity 21 Sleep, mood and social life 19 Hearing and vision 8 Alcohol, tobacco and cannabis 6 Infection and vaccination 5 Heart and metabolic health 4 Injury, delirium and falls 4 Environment 3 Cognitive activity 2
Question Both Prevention 190 Treatment 192
Direction Any Benefit 144 Harm 105 No effect 38 Mixed 37 No direction reported 58
Design Any meta-analysis 57 randomised trial 44 phase 3 trial 15 systematic review 9 phase 2 trial 10 cohort study 136 phase 1 trial 2 cross-sectional study 31 case-control study 14 modelling study 20 regulatory decision 7 company announcement 1 coverage determination 1 None 35
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Showing 2 of 382 rows. One row per study per exposure: a study that tested two different things appears twice, once for each.

Scroll the table sideways to see every column.

Research and outcomes, 2 rows. Every row links to its source.
Exposure Question Direction Outcome measured Design People Effect size, as the source reported it Source
APOE genotype Genes (not modifiable) Prevention Benefit
why

Direction 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
Rare protective or risk variant (APOE3 Christchurch, APOE R145C, RELN, FN1) Genes (not modifiable) Prevention Benefit
why

Direction 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

How this table was built, and where it is weak →