Every finding in the evidence table: 382 rows, filterable

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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

Showing 7 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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Research and outcomes, 7 rows. Every row links to its source.
Exposure	Question	Direction	Outcome measured	Design	People	Effect size, as the source reported it	Source
Birth cohort and calendar period (secular trend in dementia) All modifiable factors together	Prevention	Benefit why Direction is for more recent birth cohort: after controlling for age and period, later-born cohorts were less likely to have dementia in all three regions, more so among women; the point estimates for men in England were not significant.	Age-specific dementia prevalence by birth cohort in the US, Europe and England	cross-sectional study	62,437	point estimate for 1944-1948 vs 1919-1923 cohorts: US, -0.55 [95% CI, -0.77 to -0.34] vs -0.18 [95% CI, -0.25 to -0.10]; Europe, -1.49 [95% CI, -1.72 to -1.27] vs -0.24 [95% CI, -0.35 to -0.13]; and England, -0.48 [95% CI, -0.89 to -0.08] vs -0.23 [95% CI, -0.38 to -0.07]	JAMA Network Open 2025 ✓ Peer-reviewed PMID 40455442
Birth cohort and calendar period (secular trend in dementia) All modifiable factors together	Prevention	Benefit why Direction is for the later survey year: prevalence fell from 11.6% to 8.8%, with rising education associated with some of the decline despite a worse cardiovascular risk profile.	Dementia prevalence among US adults 65+, 2000 versus 2012	cross-sectional study	21,057	Dementia prevalence among those 65 years or older decreased from 11.6% (95% CI, 10.7%-12.7%) in 2000 to 8.8% (95% CI, 8.2%-9.4%) (8.6% with age- and sex-standardization) in 2012 (P < .001)	JAMA Internal Medicine 2017 ✓ Peer-reviewed PMID 27893041
Birth cohort and calendar period (secular trend in dementia) All modifiable factors together	Prevention	Benefit why Direction is for the later-born population: prevalence was 6.5% against the 8.3% expected from the earlier study (odds ratio 0.7), which the authors read as a cohort effect.	Dementia prevalence at age 65+ in three English areas, CFAS II (2008-11) versus CFAS I (1989-94)	cross-sectional study	15,431	Using CFAS I age and sex specific estimates of prevalence in individuals aged 65 years or older, standardised to the 2011 population, 8·3% (884,000) of this population would be expected to have dementia in 2011. However, CFAS II shows that the prevalence is lower (6·5%; 670,000), a decrease of 1·8% (odds ratio for CFAS II vs CFAS I 0·7, 95% CI 0·6-0·9, p=0·003)	The Lancet 2013 ✓ Peer-reviewed PMID 23871492
Sex differences (biological sex as exposure) All modifiable factors together	Prevention	Harm why Direction is for female sex: women had higher odds of a high neuritic plaque burden than men after adjustment, and were more likely to reach Braak stage V-VI. Black non-carriers and non-carriers of African ancestry were least likely to have high plaque burden, a protection weakened in ε4 carriers.	Neuritic plaque burden (CERAD score) at autopsy by sex, and its interaction with APOE ε4, race and African ancestry	cross-sectional study	2,268	Female individuals had higher plaque burden than male individuals (unadjusted odds ratio [OR], 1.97; 95% CI, 1.67-2.29; P < .001), and this association remained significant in adjusted models for sociodemographic and vascular factors and APOEε4 status (adjusted OR, 1.65; 95% CI, 1.33-2.20; P < .001). APOEε4 carriers of both sexes had an approximately 4-fold greater odds of plaques	JAMA neurology 2026 ✓ Peer-reviewed PMID 41729539
Blood biomarker test (p-tau217 / amyloid ratio) Care, carers and services	Prevention	Benefit why Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Stand-alone plasma p-tau217 gave 81% accuracy and 79% PPV; confirming positives with PET or CSF raised both to 91% while cutting PET scans needed to find 100 amyloid-positive people from 536 to 124. Immunoassays matched mass spectrometry on PPV but had lower accuracy.	Accuracy and positive predictive value for amyloid positivity (CSF or PET) in cognitively unimpaired people, stand-alone and in a two-step workflow	cross-sectional study	2,916	As a stand-alone test, plasma p-tau217 achieved a positive predictive value (PPV) of 79% (95% CI, 74-84) and an overall accuracy of 81% (95% CI, 80-82). In a 2-step workflow, the PPV and accuracy significantly increased to 91% (95% CI, 86-95). While this approach required screening of 677 individuals with plasma p-tau217 to identify 100 Aβ-positive individuals, compared to 536 participants when using PET alone, it reduced the need for PET testing to 124	JAMA Neurology 2025 ✓ Peer-reviewed PMID 40952756
APOE genotype Genes (not modifiable)	Prevention	No direction reported why A 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
Polygenic risk / GWAS loci Genes (not modifiable)	Prevention	No direction reported why A transcriptome-wide association study prioritising nine genes (including BIN1, PTK2B and DMPK) with broadly consistent effects across populations; it reports no effect estimate for any exposure, so no direction is recorded.	Genes whose blood expression is genetically associated with Alzheimer's disease across three populations	cross-sectional study	751	not established — pubmed abstract reports gene counts and a correlation (r2 ≈ 0.34 between two bin1 variants), no effect estimate.	American Journal of Human Genetics 2026 ✓ Peer-reviewed PMID 42066773

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