A study from the Rensselaer Polytechnic Institute, Biological Sciences, looked into how the brain cleared a harmful protein linked to Alzheimer’s disease
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Practically every function of the body and every organ within it is on a 24-hour clock of waking and sleeping.
In particular, we’ve come to realise the crucial nature of getting sound sleep, due to its affects on appetite, weight and insulin sensitivity.
And now a new benefit of sleep has been revealed – the possibility it could help stop Alzheimer’s.
A much-quoted reason for why we sleep is it gives the brain the time and opportunity to jettison a lot of rubbish.
A study from the Rensselaer Polytechnic Institute, Biological Sciences, in Troy, New York, looked into how the brain cleared a harmful protein linked to Alzheimer’s disease.
The findings provide a possible explanation for the link between Alzheimer’s disease and disruptions to a person’s sleep.
It is becoming clear that a healthy sleep pattern may be important to ease some symptoms of the disease.
Moreover, the study suggests good sleep is important in preventing the protein – known as amyloid-beta 42 (AB42) – from forming destructive clumps in the brain, and could be the basis of potential therapies for Alzheimer’s.
This would mean during sound sleep the rogue proteins could be cleared out of the brain. The likelihood of developing Alzheimer’s could also be less and symptoms less severe.
Alzheimer’s disease is known to be associated with disruptions in circadian rhythms, the 24-hour cycle (body clock) that controls many aspects of our behaviour and physiology.
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Sleep disturbances start years before symptoms appear and are linked to greater severity of the disease and a higher risk of developing it, previous research has found.
Associate professor Jennifer Hurley, an expert in circadian rhythms at Rensselaer Polytechnic Institute, says: “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 AB42 in the brains of people with Alzheimer’s disease.
They found they cleared away the AB42 on an oscillating daily cycle controlled by circadian rhythms.
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 findings present the possibility that, if the 24-hour clearance of AB42 can be maintained, patients may be less likely to develop Alzheimer’s disease and have less severe symptoms.