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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
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

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