Every finding in the evidence table: 382 rows, filterable

Every row

Filter

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 10 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, 10 rows. Every row links to its source.
Exposure	Question	Direction	Outcome measured	Design	People	Effect size, as the source reported it	Source
Omega-3 / fish and fish oil Diet and supplements	Prevention	Mixed why The biochemical primary outcome was met (DHA raised the CSF DHA-to-arachidonic-acid ratio versus placebo), but there was no difference in cognition or brain volume over 24 months. The authors recommend against further supplementation trials of this kind.	CSF DHA/AA ratio at 6 months (primary, target engagement); cognition and brain volumes at 24 months	phase 2 trial	365	DHA supplementation increased CSF DHA/AA ratio at 6 months vs placebo (0.17 [95% CI 0.15-0.18] vs -0.02 [95% CI -0.04 to -0.0004]; difference 0.19 [95% CI 0.16-0.21]; p < 0.0001), independent of APOE ε4 status (interaction p = 0.71). Dropout was 38%, mainly due to COVID-19. No treatment differences were observed in brain volumes or cognitive performance over 24 months	EBioMedicine 2026 ✓ Peer-reviewed PMID 42315445
Anti-amyloid antibody Medicines	Treatment	Benefit why Phase Ib/IIa biomarker result in 13 people; no cognitive outcome measured.	Amyloid PET and CSF biomarkers (surrogate)	phase 2 trial	13	3.6 mg/kg cohort: "-89 centiloids after 12 weeks (n=13), and -107 centiloids after 28 weeks (n=12)" on amyloid PET; at week 25 CSF "total tau, phosphorylated tau181, and neurogranin were reduced by 30%, 34%, and 29%, respectively"	Alzheimer's & Dementia (AAIC 2025 conference abstract) 2025 ⚠ Conference abstract — not peer-reviewed PMC12740797
Anti-tau therapy Medicines	Treatment	No effect why The primary endpoint was not met: the low dose showed no clinically meaningful benefit and the 3 mg dose showed 32% greater progression than placebo, with more serious adverse events. Less whole-brain volume loss on MRI is a surrogate finding.	iADRS disease-progression ratio at 100 weeks (primary); tau PET, brain volume, adverse events	phase 2 trial	327	The disease progression ratio relative to placebo was 0.84 (95% credible interval [CrI], 0.66-1.04) for the ceperognastat 0.75 mg group and 1.32 (CrI, 1.10-1.58) for the ceperognastat 3 mg group, corresponding to 16% less and 32% greater progression, respectively. No benefits were demonstrated for secondary clinical end points	JAMA 2026 ✓ Peer-reviewed PMID 42441396
Anti-tau therapy Medicines	Treatment	No effect why The primary clinical endpoint (CDR-SB) was not met in the overall population. The tau figures are a biomarker outcome, not a clinical one.	CDR-SB (primary); tau PET accumulation	phase 2 trial	466	"Slowed the rate of tau accumulation versus placebo in key brain regions by 33%-58%" overall and "by 63%-67%" in the low-tau or APOE4 non-carrier subgroup; "In the overall study population, no beneficial effect of low- or high-dose bepranemab compared with placebo was observed on the primary endpoint"; ADAS-Cog14 decline slowed 21-25%	UCB press release (data presented at CTAD 2024) 2024 ⚠ Press release — not a study no DOI or PMID exists
Anti-tau therapy Medicines	Treatment	No effect why ADAS-Cog11 showed slower decline, but the co-primary functional endpoint (ADCS-ADL) did not differ and the authors classify the study as negative.	ADCS-ADL and ADAS-Cog11 (co-primary) at week 49	phase 2 trial	272	"At week 49, the semorinemab arm demonstrated a 42.2% reduction (-2.89 points, 95% CI -4.56 to -1.21, p = 0.0008) in decline on the ADAS-Cog11 (coprimary endpoint) relative to the placebo arm"; ADCS-ADL difference -0.83 points (95% CI -3.39 to 1.72, p = 0.52), with no difference on MMSE or CDR-SB	Neurology 2023 ✓ Peer-reviewed PMID 37643887
Antiviral (valacyclovir) for HSV-seropositive Alzheimer's Medicines	Treatment	Harm why Direction is for valacyclovir: cognition worsened more on the drug than on placebo on the primary outcome (between-group difference 3.93 ADAS-Cog points, P = .01); function, amyloid PET and tau PET did not differ. The authors conclude it is not recommended.	ADAS-Cog change at 78 weeks (primary); ADCS-ADL, amyloid PET and tau PET	phase 2 trial	120	At 78 weeks, the LSM change in the 11-item ADAS-Cognitive Subscale score was 10.86 (95% CI, 8.80 to 12.91) in the valacyclovir group vs 6.92 (95% CI, 4.88 to 8.97) in the placebo group, indicating greater cognitive worsening with valacyclovir than placebo (between-group difference, 3.93 [95% CI, 1.03 to 6.83]; P = .01). The LSM change in the ADCS-ADL Scale score at 78 weeks was -13.78 (95% CI, -17.00 to -10.56) in the valacyclovir group vs -10.16 (95% CI, -13.37 to -6.96) in the placebo group (between-group difference, -3.62 [95% CI, -8.16 to 0.93])	JAMA 2026 ✓ Peer-reviewed PMID 41405855
GLP-1 receptor agonist Medicines	Treatment	No effect why Primary outcome null. One secondary cognitive measure (ADAS-Exec) favoured liraglutide on an unadjusted test; ADCS-ADL and CDR-SB did not.	Cerebral glucose metabolic rate at 52 weeks (primary)	phase 2 trial	204	Cerebral glucose metabolism difference -0.17 (95% CI -0.39 to 0.06, p=0.14); CDR-SB -0.06 (95% CI -0.57 to 0.44)	Nature Medicine 2026 ✓ Peer-reviewed PMID 41326666
Other investigational drug Medicines	Treatment	No effect why The trial did not meet its primary endpoint at any of three doses despite sustained target engagement (lower CSF soluble TREM2, higher osteopontin); the most frequent adverse events were MRI changes resembling ARIA.	Change from baseline in CDR-SB at week 96 versus placebo (primary endpoint) with the TREM2 agonist antibody AL002	phase 2 trial	381	least squares mean difference versus placebo (95% confidence interval) at week 96: 15 mg kg-1 -0.31 (-1.61 to 0.98), 40 mg kg-1 0.13 (-1.18 to 1.43) and 60 mg kg-1 -0.17 (-1.49 to 1.15); P > 0.05 from mixed-effects model for repeated measures	Nature Medicine 2026 ✓ Peer-reviewed PMID 41787076
Psychotropics for agitation / psychosis Medicines	Treatment	Benefit why The NPI-C agitation/aggression measure did not reach significance (p=0.094).	Pittsburgh Agitation Scale over 3 weeks	phase 2 trial	75	PAS decline difference -0.74/week (p=0.015, ES 0.53); NPI-C A/A -1.26/week (p=0.094, ES 0.36)	The American Journal of Geriatric Psychiatry 2026 ✓ Peer-reviewed PMID 41350162
Psychotropics for agitation / psychosis Medicines	Treatment	Benefit why The authors describe the reduction as small (-1.32 points).	NPI apathy score at 6 weeks	phase 2 trial	94	NPI apathy change -1.32 points (95% CI -2.43 to -0.21) vs placebo	The Lancet Neurology 2025 ✓ Peer-reviewed PMID 39862881

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

Every row of the evidence table

Every row