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.

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.

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).

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.

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.