Sleepiness in Alzheimer’s patients is caused by damage to neurons that help us stay awake

Sleepiness in Alzheimer’s patients is caused by damage to neurons that help us stay awake

The finding could lead to new treatments to help those with the disease to stay more alert.

Published: April 4, 2022 at 3:33 pm

Frequent napping during the daytime 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, a team of 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 neurons found in brain areas known to 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 stablise 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) during their stay and donated their brains to be used for research after they died.

They compared the brains of 33 patients with Alzheimer’s to 20 who had progressive supranuclear palsy (PSP), a neurodegenerative condition that leaves patients unable to sleep, and 32 patients who had healthy brains until the end of their lives.

They found that neurons in the three brain areas being studied are responsible for producing neurotransmitters that either excite or inhibit other nerve cells and lead to feelings of sleepiness or 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 co-author Joseph Oh, a medical student at the University of California.

“Finally, with this post-mortem 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 indicates that treatments to help regulate sleep patterns in patients with Alzheimer’s may be created by developing a method of bumping up the ‘awake’ system and damping down the ‘sleep’ system, the researchers say.

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