The finding could lead to new treatments for those with the disease to help them stay alert
Frequent napping during the day is a common symptom of Alzheimer’s and can begin long before any of the memory problems associated with the disease occur. It was widely believed that this was due to patients suffering from periods of disturbed sleep at night and subsequently needing to catch up by taking daytime naps.
Now, researchers based at the University of California, San Francisco, have discovered that the lethargy and sleepiness experienced by Alzheimer’s patients is due to damage to the neurons found in brain areas that promote wakefulness, namely the locus coeruleus, the lateral hypothalamic area and the tuberomammillary nucleus. This damage is caused by the accumulation of tau proteins – small molecules that usually help to stabilise the structure of neurons but break free and clump together in the brains of those with Alzheimer’s.
The team made the discovery after studying data taken from patients at the university’s Memory and Aging Center, who volunteered to have their sleep monitored with an electroencephalogram (EEG) and donated their brains to be used for research after they died.
The brains of 33 patients with Alzheimer’s were compared to 20 who had progressive supranuclear palsy (PSP), a neurodegenerative condition that leaves patients unable to sleep.
They found that neurons in the three brain areas are responsible for producing neurotransmitters. In Alzheimer’s patients, these neurotransmitters then inhibit other nerve cells, leading to feelings of sleepiness. In PSP patients, they excite them, causing wakefulness.
“You can think of this system as a switch with wake-promoting neurons and sleep-promoting neurons, each tied to neurons controlling circadian rhythms,” said Joseph Oh, a medical student and one of the lead authors. “With this postmortem tissue, we’ve been able to confirm that this switch, which is known to exist in model animals, also exists in humans and governs our sleep and awake cycles.”
The finding could lead to treatments that bump up the ‘awake system’ in Alzheimer’s patients.