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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 11 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, 11 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
APOE genotype Genes (not modifiable)	Prevention	Harm why Direction 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 why Direction 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 APOE34 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 APOE22+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
Polygenic risk / GWAS loci Genes (not modifiable)	Prevention	No direction reported why Locus-discovery genome-wide association study: it reports which genetic regions reached significance and no effect estimate for any exposure, so no direction is recorded. Nine signals (HP1BP3, SLC50A1, PTPRC, NPAS3, DDHD1, CHST9, SMYD2, PRAMEF1, GFRA1) appeared only in APOE-stratified analyses; DDHD1 was protective in ε4 carriers.	New genome-wide risk loci for AD found when stratifying by APOE ε4 and ε2 carrier status	case-control study	not stated	not established — the abstract names nine new loci and prints no effect estimate.	Nature genetics 2026 ✓ Peer-reviewed PMID 42736378
Polygenic risk / GWAS loci Genes (not modifiable)	Prevention	No direction reported why Locus-discovery genome-wide association study: it reports which genetic regions reached significance and no effect estimate for any exposure, so no direction is recorded. The study reports eight new loci (six ancestry-specific, two trans-ancestry) and nominates eight genes in microglial activation, glutamate production and signalling.	Genome-wide significant loci for early-onset Alzheimer's disease (onset before 70)	case-control study	25,236	not established — pubmed abstract reports locus counts and pathways, no effect estimate.	Alzheimer's & Dementia 2025 ✓ Peer-reviewed PMID 40556318
Polygenic risk / GWAS loci Genes (not modifiable)	Prevention	No direction reported why Locus-discovery genome-wide association study: it reports which genetic regions reached significance and no effect estimate for any exposure, so no direction is recorded. Beyond APOE, the study reports TREM2 R47H and variants near RAB3B, SPOCK3/ANXA10 and SMAP2, and a gene-based association with GIPR.	Genome-wide and exome-wide loci for Alzheimer's disease in Ashkenazi Jews	case-control study	not stated	not established — pubmed abstract reports p-values for the loci and no effect estimate.	Alzheimer's & Dementia 2023 ✓ Peer-reviewed PMID 37260021
Polygenic risk / GWAS loci Genes (not modifiable)	Prevention	No direction reported why Locus-discovery genome-wide association study: it reports which genetic regions reached significance and no effect estimate for any exposure, so no direction is recorded. Two signals at 17p13.2 and 18q21.33 are reported; the authors state that African ancestry at 17p13.2 went with lower AD risk and that overall African ancestry did not differ between cases and controls, without an effect estimate.	Admixture-mapping loci for Alzheimer's disease in African Americans	case-control study	10,271	not established — pubmed abstract reports p-values for the two loci and no effect estimate.	Alzheimer's & Dementia 2023 ✓ Peer-reviewed PMID 36539198
Polygenic risk / GWAS loci Genes (not modifiable)	Prevention	Mixed why The study's own results point different ways: the polygenic score added to APOE for predicting AD/MCI and for progression from amyloid-positive MCI to AD, but amyloid deposition was predicted by APOE alone.	Prediction of AD, MCI, amyloid deposition and MCI-to-AD progression (AUC) by polygenic risk score with and without APOE	case-control study	770	AD and MCI are predicted by both APOE genotype and PRS (area under the curve [AUC] = 0.82% and 68%, respectively). Amyloid deposition is predicted by APOE only (AUC = 79%). Further progression to AD of individuals with MCI and amyloid-positive status is predicted by PRS over and above APOE (AUC = 67%)	Annals of Neurology 2019 ✓ Peer-reviewed PMID 31199530
Rare copy-number variants (22q11.21 dosage, ABCA1 / ABCA7 deletions) Genes (not modifiable)	Prevention	Mixed why The two kinds of variant point opposite ways: deletions and loss-of-function alleles in ABCA1 and ABCA7 and 22q11.21 deletions raised AD risk, while 22q11.21 duplication lowered it (odds ratio 0.34 at exome-wide significance in replication). Not modifiable.	Alzheimer's disease case status (early- and late-onset) by rare copy-number variant burden and 22q11.21 dosage	case-control study	22,319	ABCA1 (odds ratio [OR] = 5.77 [95% confidence interval 2.25; 17.06], p = 0.0002) and ABCA7 deletions contribute to this deletion burden (OR = 2.29 [1.44; 3.65], p = 0.0006), while CTSB LoF alleles appear as candidates (OR = 5.03 [1.50; 20.71], p = 0.0089) ... Replication in 33,977 affected individuals and 362,322 control subjects confirmed association for 22q11.21 dosage with exome-wide significance (ORSCARF2 = 0.34 [0.21; 0.53]; mega-p value = 5.52 × 10-7)	American Journal of Human Genetics 2026 ✓ Peer-reviewed PMID 42648288
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
Rare protective or risk variant (APOE3 Christchurch, APOE R145C, RELN, FN1) Genes (not modifiable)	Prevention	Harm why Direction is for carrying the African ancestry-specific APOE R145C variant with an ε3/ε4 genotype: three-fold higher odds of AD and onset about six years earlier in the discovery stage, replicated in stage 2 and concordant in stage 3. Not modifiable.	Alzheimer's disease case status and age at onset among APOE ε3/ε4 carriers of African ancestry	case-control study	31,929	R145C was associated with an increased risk of AD (odds ratio [OR], 3.01; 95% CI, 1.87-4.85; P = 6.0 × 10-6) and was associated with a reported younger age at AD onset (β, -5.87 years; 95% CI, -8.35 to -3.4 years; P = 3.4 × 10-6)	JAMA 2023 ✓ Peer-reviewed PMID 36809323

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