Every row of the evidence table

Incidence was consistently but non-significantly lower in the 2000 subcohort (rate ratio 0.75, 95% CI 0.56-1.02, borderline). The authors read the pattern, together with lower mortality and larger brain volumes, as suggesting a decline, but the primary comparison did not reach significance.

Direction is for the blood test's ability to detect treatment-related amyloid clearance on PET: AUC 0.61, which the authors call suboptimal and not currently usable for that purpose. It says nothing about the drug's effect.

No significant difference in 5-year cumulative spending between spouses of people with and without dementia ($3,974, 95% CI -$3,199 to $11,477); year-5 spending was higher (+$2,748), driven by inpatient costs.

No difference from waitlist control on the primary burden outcome or on mood, WHOQOL-Bref or productivity; only the CarerQoL-VAS quality-of-life score was higher in the intervention group. The trial recruited 93 of a 194 target.

Burden fell in both arms with no significant difference between the two platforms. There was no untreated control, so the within-arm improvement cannot be separated from time or attention.

No difference between health-system care, community-based care or usual care on either primary outcome. Caregiver self-efficacy did improve in both active arms.

No benefit and no harm: screening did not change family-member quality of life, preparedness or self-efficacy, and did not raise depression or anxiety. Only 5.1% screened positive.

Difference-in-differences around ACO entry found no change in end-of-life care processes, outcomes or spending.

The primary outcome did not improve. Emergency department visits and hospitalisations were lower (RR 0.45, 95% CI 0.31-0.65), which is a secondary outcome.

Three trials comparing respite with no respite found no significant benefit on any carer outcome; the four included trials were too different to pool.

Neither the combined package nor risk-factor modification beat health advice.

The control arm also received diet counselling and mild caloric restriction, so this is MIND against another active diet, not against usual eating. It is the only randomised test of the MIND diet here and it disagrees with the cohort evidence.

The control arm also received diet counselling and mild caloric restriction, so this is MIND against another active diet, not against usual eating. It is the only randomised test of the MIND diet here and it disagrees with the cohort evidence.

Risk ratios close to one across every intake strategy, including substituting fish for meat. This is the one study here that emulates a trial rather than comparing eaters with non-eaters, and it disagrees with the pooled cohorts.

The intervention did not change any brain biomarker trajectory. Participants with lower baseline hippocampal volume did show a greater cognitive benefit.

A small improvement that did not reach significance (adjusted difference 0.06, 95% CI -0.001 to 0.128, p=0.055).

No difference between aerobic training and stretching/balance. Cognition was stable in both arms, but with no non-exercising control the trial cannot say whether either arm helped.

Neither the combined package nor risk-factor modification beat health advice.

Explicitly finds no neuroprotective effect, and attributes the lower risk seen in other cohorts to reverse causation: activity fell in the nine years before diagnosis. This contradicts the pooled cohort evidence.

The primary outcome did not move between groups. Attention and inhibitory control did improve (SMD 0.43), as did muscular strength.

Null in the primary analysis of the whole cohort. The prespecified analysis of the higher-risk ARIC subgroup found less decline, which the authors present as hypothesis-generating rather than as a result.

Co-primary endpoints were not met at 52 weeks. The comparator was a low dose of the same drug rather than placebo, which the authors say masked any separation; they report separation in the MCI subgroup only at 78 and 104 weeks.

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.

The primary clinical endpoint (CDR-SB) was not met in the overall population. The tau figures are a biomarker outcome, not a clinical one.

ADAS-Cog11 showed slower decline, but the co-primary functional endpoint (ADCS-ADL) did not differ and the authors classify the study as negative.

No difference from placebo on the primary agitation outcome or other main behavioural outcomes. As-needed psychotropic use was lower during the active period, and no serious drug-related adverse events occurred.

The authors state the data are compatible with anything from a 39% decrease to a 5% increase in risk, against DPP-4 inhibitors rather than no treatment.

For GLP-1 receptor agonists specifically: HR 0.95 (95% CI 0.87-1.04) against DPP4 inhibitors in the intention-to-treat analysis. Only the continuous-use analysis reached significance (HR 0.79).

Primary outcome null. One secondary cognitive measure (ADAS-Exec) favoured liraglutide on an unadjusted test; ADCS-ADL and CDR-SB did not.

Designed around new diabetes diagnoses with a landmark analysis and a one-year lag, which removes the prevalent-user advantage that inflates metformin's apparent benefit in the pooled cohorts.

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.

Not effective, and drug-related QT prolongation was observed. The randomised sample was smaller than planned.

After the first year the data rule out more than a 3% change either way. Diagnoses were 46% higher in the first year, which the authors attribute to people being seen more often just after starting a statin. This sits against the Chicago cohort, which found benefit in APOE4 carriers.

Midlife depressive symptoms did not raise dementia risk (HR 1.21, 95% CI 0.95-1.54), even when chronic. The association closer to diagnosis is read by the authors as depression being a prodromal feature, not a cause.

Neither choir singing nor group music therapy beat standard care. Country was the strongest predictor of the differences between sites.