Every row of the evidence table

Compared with flexible health advice, not with nothing; both groups improved.

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

Both groups improved; the structured programme improved more. The trial compares two active interventions, so there is no untreated comparison.

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

High overall and leisure-time activity were associated with lower dementia risk, but occupational and commuting activity were associated with higher risk. Certainty of evidence was very low to low.

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.

Concentrating activity into one or two days worked about as well as spreading it across the week.

Direction is for 12 weeks of cycle-ergometer exercise: putative glymphatic influx in the putamen and meningeal lymphatic vessel size and flow increased, and inflammation-related plasma proteins fell in step with the imaging changes. A mechanistic imaging result, not a cognitive outcome.

The authors call the association weak (RR 0.97), and it was absent beyond 10 years of follow-up.

Pooled across 29 cohorts. The association weakened to HR 0.85 after maximal confounder adjustment and was not significant for low-intensity activity.

The authors state the association held in longer follow-ups, which is their answer to the reverse-causation objection raised by the Whitehall II cohort.

866 cases over a short follow-up for a disease with a long prodrome, so some of the association may be people already declining moving less.

The largest effect for physical activity anywhere in this table by a wide margin. On 678 cases over 6.3 years, in a disease with a long prodrome, reverse causation is the more likely explanation for an effect that size.

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.

Pools 27 small trials in people who already have dementia, and reports a much larger effect (SMD 0.69) than the single largest such trial, DAPA, which found none.

The primary cognitive outcome was significantly WORSE in the exercise arm (adjusted difference -1.4, 95% CI -2.6 to -0.2, favouring usual care). The authors conclude the programme does not slow cognitive impairment and treat the difference as of uncertain clinical importance. Fitness did improve. This is the sharpest counterweight to the observational exercise evidence.

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

The authors call the effect small (-0.18 points). Significant in women, not in men, on 91 randomised and 76 completing.

Seven small trials; working memory did not improve (P=0.14).