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.

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.

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 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.