So neurovascular coupling is more immediately sensitive to physical activity level - but maybe changes in basal neurovascular function take longer to develop? Better keep up that exercise routine (she says, hypocritically)!

Anyway thanks again team and to you for reading!

But what it does suggest, is that exercise might particularly protect APOE4 carriers by protecting neurovascular function. So let's all go to the gym!

In sedentary APOE4 mice, neurons can't increase their blood flow very well when neurons are active - over time could this mean neurons don't get enough energy, promoting Alzheimer's disease?

And the reduction in neurovascular function in these APOE4 sedentary mice was biggest when neurons were active - when they are using more energy so need more blood flow. So there's a bigger effect when the system is under pressure.

But mice with the genetic risk factor for AD - APOE4 - were especially sensitive to exercise. The worst neurovascular function was consistently seen in APOE4 sedentary mice.

She measured *loads* of different aspects of neuronal and vascular function (e.g. calcium signals in neurons, blood flow, blood oxygen, how well different vessels dilate) Generally more active mice had better neurovascular function, and less active mice had worse.

Silvia tested this by comparing neurovascular function in APOE4 (increased AD risk) and APOE3 (normal AD risk) mice but in some mice she took their exercise wheel away!! These mice were indeed less active.

But others studying anaesthetised mice found big effects of APOE4 on blood vessels. Why the difference? Well, Orla's mice were super-fit and healthy with an exercise wheel in their cage. Exercise protects from dementia - were Orla's mice' blood vessels protected?

UPDATE!! We have spent a long time fashioning bits with floristry wire!

Classic Christmas.