Alzheimer’s disease: Drowsiness could signal damage to cells that keep the body awake
Alzheimer's: Dr Chris discusses the early signs of condition
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Rates of Alzheimer’s disease are climbing sharply year on year, but treatments are only able to soften symptoms. One of the complications harder to manage is fatigue, which affects patients in the initial and late stages of Alzheimer’s. But new research has shed light on the potential mechanisms at play, which could prove instrumental in the development of a suitable treatment.
Alzheimer’s disease is characterised by a plethora of symptoms, including wandering, becoming agitated, and acting overly suspicious.
In the initial stages of the condition, however, a high number of patients describe low energy levels.
Health bodies state that the symptom can be as hard to manage as memory loss and confusion.
This is why many patients need far more sleep than they’re used to, and appear more fatigued upon waking.
READ MORE: Alzheimer’s breakthrough: Study identifies 42 genes linked to condition
To date, most researchers have credited the sleep problems to an accumulation of beta-amyloid protein in the brain.
But new research has suggested the probable cause is damage to the neurons that control wakefulness.
Neuropathologist Grinderg, who authored the study alongside psychiatrist Thomas Neylan, said: “We were able to prove what our previous research had been pointing to – that in Alzheimer’s patients who need to nap all the time, the disease has damaged the neurons that keep them awake.
“It’s not that these patients are tied during the day because they didn’t sleep at night. It’s that the system in their brain that would keep them away is gone.
“We see that these patients can’t sleep because there is nothing telling the ‘awake’ neurons to shut down.
“Now rather than trying to undo these people to sleep, the idea is to shut down the system that’s keeping them awake.”
The data that formed the basis of this argument came from participants at UC San Francisco’s Memory and Ageing Centre, who volunteered to have their sleep monitored and donate their brains after they died.
The study looked at the brains of 33 patients with Alzheimer’s disease, 20 with progressive supranuclear palsy (PSP) and 30 controls.
Levels of two proteins associated with dementia, beta-amyloid and tau, were measured in all patients.
The findings highlighted that in conditions where the sleep neurons become damaged, such as PSP, patients tend to become sleep deprived because they are unable to sleep.
The team hypothesised that patients with Alzheimer’s experience trouble staying awake after neurons that keep them awake become damaged at the onset of the disease.
Joseph Oh, a medical student and one of the study’s other authors, said: “You can think of this system as a switch with wake-promoting neurons and sleep-promoting neurons, each tied to neurons controlling the circadian rhythm.
“Finally, with this post-mortem tissue, we’ve been able to confirm that this switch, which is known to exist in modern animals, also exists in humans and governs our sleep and wake cycles.”
Sleep is crucial in the prevention of Alzheimer’s disease because it is during sleep that waste matter is flushed from the brain.
The findings appear to indicate that treatments for Alzheimer’s could be altered on the basis of each patient’s needs, as some may need their awake system boosted or their sleep system tamped down.
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