The findings provide a potential explanation for the link between the disease and disruptions to a person’s sleep cycle.
10 February 2022
The brain’s ability to clear a protein closely linked to Alzheimer’s disease is linked to the body’s 24-hour clock, a new study suggests.
The findings provide a potential explanation for the association between Alzheimer’s disease and disruptions to a person’s sleep cycle.
Research suggests a healthy sleep pattern might be important to ease some symptoms of the disease.
And according to the experts, the new study highlights the importance of good sleep in preventing a protein – known as Amyloid-Beta 42 (AB42) – from forming clumps in the brain, and opens a path to potential therapies for Alzheimer’s.
The findings present the possibility that if the proteins can be cleared daily, people may be less likely to develop Alzheimer’s disease and to exhibit less severe symptoms, according to experts.
Alzheimer’s disease is known to be associated with disruptions in circadian rhythms, the 24-hour cycle that controls many aspects of human behaviour and physiology.
Sleep disruptions start years before symptoms appear and are linked to more severe symptoms and a higher risk of developing the disease, previous research has found.
Jennifer Hurley, an expert in circadian rhythms, and associate professor of biological science at Rensselaer Polytechnic Institute, America, said: “Circadian regulation of immune cells plays a role in the intricate relationship between the circadian clock and Alzheimer’s disease.
“This tells us a healthy sleep pattern might be important to alleviate some of the symptoms in Alzheimer’s disease, and this beneficial effect might be imparted by an immune cell type called macrophages/microglia.”
Researchers measured the activity of immune cells responsible for clearing away the protein that builds up as plaques in the brains of people with Alzheimer’s disease.
They found that the immune cells cleared away the amyloid-beta on an oscillating daily cycle controlled by circadian rhythms.
However, when cells lost that rhythm, the daily cycle disappeared.
Dr Hurley said: “In theory, if we could boost that rhythm, perhaps we could increase the clearance of AB42 and prevent damage to the brain.”
The study further suggested the underlying cause of this oscillation was changes in the number of molecules of a certain protein on the cell’s surface.
The protein, called heparan, which responds to circadian rhythms had previously been shown to play a role in clearing amyloid-beta proteins, researchers say.
Researchers uncovered a mechanism that links the disruption of circadian rhythms to Alzheimer’s disease, and the study highlights the role of immune cells in this relationship.
According to the scientists, while more studies are 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.
The findings are published in the PLoS Genetics journal.
