New research has pinpointed the molecular mechanism behind the relationship between Alzheimer’s Disease (AD) and sleep disruption, which researchers hope will pave the way for new preventative measures and treatments for the disease.
Dr Jennifer Hurley, alongside colleagues from New York’s Rensselaer Polytechnic Institute, found that the immune cells responsible for clearing away a key protein – that which builds up in the brains of patients with Alzheimer’s disease – operates according to daily circadian rhythms, the 24-hour cycle that controls many aspects of human behaviour and physiology.
The finding, recently published in PLOS Genetics, provides a potential explanation for the link between Alzheimer’s disease and disruptions to a person’s sleep cycle.
Sleep disruption can lead to the disruption of circadian rhythms in our immune cells, which could play a role in an increase in the risk and severity of Alzheimer’s disease.
Dr Jennifer Hurley, researcher, New York’s Rensselaer Polytechnic Institute
It has been observed that sleep disruptions begin years before symptoms of Alzheimer’s disease appear and are linked to more severe symptoms and a higher risk of developing the disease; this latest research pinpoints why.
“Sleep disruption can lead to the disruption of circadian rhythms in our immune cells, which could play a role in an increase in the risk and severity of Alzheimer’s disease,” Hurley tells Aged Care News.
Throughout the study, researchers measured the activity of immune cells responsible for clearing away proteins called amyloid-beta that build up as plaques in the brains of people with Alzheimer’s disease.
Using cultures of these cells grown in the lab, they discovered that the immune cells clear away the amyloid-beta on an oscillating daily cycle controlled by circadian rhythms.
However, when cells lost that rhythm, the daily cycle disappeared, with researchers establishing that the underlying cause of this oscillation was changes in the number of molecules of a certain protein, heparan, on the cell’s surface.
The protein they identified responds to circadian rhythms and previously had been shown to play a role in clearing amyloid-beta proteins.
From this, researchers deduced that implementing improvements to one’s “sleep hygiene” may have a noticeable improvement on one’s susceptibility to the disease and/or its progression.
“Our study suggests that good sleep hygiene, that is no bright lights at night, no TVs on while you sleep, etc, over a life span may help with the accumulation of Amyloid beta by helping to keep your circadian rhythms aligned.”
To Aged Care News‘ question of whether common psychotropic interventions, such as prescription sleeping tablets, would work to restore circadian cycle disruption, Hurley notes that, as a doctor of philosophy (in Molecular Genetics, Microbiology and Immunology), she avoids prescriptive comments regarding medical intervention.
“… but in general sleep, medications do not necessarily equal good sleep hygiene or the proper timing of one’s circadian rhythms.”
Furthermore, Hurley cautions that a perfect sleep schedule cannot always guarantee a reduction in plaque accumulation; circadian disruption can present more subtly.
“Our study suggests that if there is an underlying disfunction in the circadian clock of our immune cells, regardless of its effect on sleep, it could increase the risk/severity of Alzheimer’s disease,” Hurley says.
While more studies will be necessary, the new findings present the possibility that, if the daily clearance of amyloid-beta proteins through this mechanism can be maintained, patients may be less likely to develop Alzheimer’s disease and to exhibit less severe symptoms.
“Understanding how our circadian rhythms can regulate cell-surface heparan levels to control the build-up of amyloid-beta may lead to the development of chronotherapeutics that alleviate the symptoms of Alzheimer’s Disease as well as other inflammatory diseases,” Hurley says.
