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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.
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Showing 5 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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| Exposure | Question | Direction | Outcome measured | Design | People | Effect size, as the source reported it | Source |
|---|---|---|---|---|---|---|---|
| Anti-tau therapy Medicines | Treatment |
No effect
whyThe 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
whyThe 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
whyADAS-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 |
| GLP-1 receptor agonist Medicines | Treatment |
No effect
whyPrimary 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
whyThe 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 |