By investigating the rhythmic behavior of immune cells and discovering the chemical ‘timers’ that govern them, scientists have discovered a probable mechanism between abnormalities in circadian rhythms as well as the build-up of proteins linked to Alzheimer’s disease.
Circadian rhythms are just the everyday rhythms of biological functions that are governed by our sleep-wake cycles and are linked to our biological body clock.
Poor sleep habits may throw circadian rhythms off (aging and stress don’t help either), and sporadic sleep means immune cells have less opportunity to clear the brain of toxins that accumulate during the day. Sleep disruptions that begin years before symptoms appear have been related to a higher chance of Alzheimer’s disease, a really prevalent type of dementia, and also more severe symptoms.
Researchers led by Rensselaer Polytechnic Institute biological scientist Jennifer Hurley looked at immune cells named macrophages, which have been shown to move further into the brain in late-stage Alzheimer’s disorder. Macrophages are foragers that eat waste materials, defective proteins, and dead cells to protect the body from harmful damage.
According to a previous study, even one night of poor sleep leads to a rise in amyloid-beta proteins, while a week of poor sleep promotes a build-up of yet another protein called tau. As a result, chronic sleep issues may be a concern.
A good first step is to identify a plausible mechanism that explains how disturbances in circadian rhythms might affect the clearing of amyloid proteins within the brain. In a roundabout way, this research contributes to other lines of inquiry such as chronotherapies, which are treatments aimed at improving people’s sleep cycles.
Studying the circadian rhythm of immune cells might have consequences for other conditions associated with inflammation, such as Alzheimer’s disease and depression.
The research was published in the PLOS Genetics journal.
