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 9 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, 9 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	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
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 14 new loci for clinically diagnosed AD and two from AD-by-proxy.	Genome-wide significant loci for clinically diagnosed AD and AD-by-proxy	meta-analysis	432,374	not established — pubmed abstract lists the loci by name and reports no effect estimate.	Alzheimer's & Dementia 2025 ✓ Peer-reviewed PMID 39998322
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
Rare protective or risk variant (APOE3 Christchurch, APOE R145C, RELN, FN1) Genes (not modifiable)	Prevention	No direction reported why A single case report: one man with the PSEN1 E280A mutation stayed cognitively intact until 67 despite very heavy amyloid, and carried a gain-of-function RELN variant. With one case and no comparison group beyond the earlier Christchurch case, no direction can be recorded.	Cognitive status and amyloid/tau burden in one PSEN1 E280A carrier heterozygous for RELN-COLBOS	None	not stated	not established — case report; the abstract reports no effect estimate.	Nature Medicine 2023 ✓ Peer-reviewed PMID 37188781
Rare protective or risk variant (APOE3 Christchurch, APOE R145C, RELN, FN1) Genes (not modifiable)	Prevention	No direction reported why Among 37 heterozygous carriers (ages 56.6-82.1) none had developed AD or MCI by the March 2022 data freeze and apolipoprotein B was lower than in non-carriers, but the authors say continued follow-up is necessary and no homozygotes were found, so protection could not be tested. No incidence comparison is reported, so no direction is recorded.	Alzheimer's disease or MCI diagnoses and blood lipid biomarkers in heterozygous APOE Christchurch carriers	cohort study	455,306	not established — research letter with no pubmed abstract; the full text at pmc10685495 reports carrier counts and p-values (apob p = 0.004; p = 0.036…	Molecular Neurodegeneration 2023 ✓ Peer-reviewed PMID 38017580

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