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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 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
why

Direction 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

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