I work in the neurotech/sleeptech space, and Alzheimer’s is one of the endpoints we’re working toward.
On a first read, it seems the authors frame everything through a circadian lens. Their view is that circadian genes regulate glial function, and that when those rhythms are disrupted, clearance breaks down, inflammation increases, and amyloid accumulates, contributing to Alzheimer’s.
There’s another perspective in sleep science that looks at restorative function. The physiological work of sleep like slow-wave activity and glymphatic flow which may be the driver. From that view, amyloid build-up impairs glymphatic clearance, creating a downward spiral of poorer clearance and more accumulation.
Circadian timing is certainly an important modulator, but it’s not the whole story. Without EEG or even basic sleep-wake data, it’s hard to know whether the changes in circadian” gene expression reported here reflect intrinsic clock disruption or simply reduced slow-wave restorative function in these mice.
I've linked to two research papers[2],[3] in AD which are working with the same principles of our work at https://affectablesleep.com
[1] https://doi.org/10.1038/s41593-025-02067-1 [2] https://doi.org/10.1016/j.jagp.2024.07.002 [3] https://doi.org/10.1093/ageing/afad228