Scientists from UC San Francisco found that the lethargy that many Alzheimer’s patients experience is caused not by a lack of sleep, but rather by the degeneration of a type of neuron that keeps us awake.
The findings contradict the common notion that Alzheimer’s patients sleep during the day to make up for a bad night of sleep and point toward potential therapies to help these patients feel more awake.
They also confirmed the tau protein is behind that neurodegeneration.
The research is published in JAMA Neurology and was conducted by Thomas Neylan et al.
In the study, the data came from study participants who were patients volunteered to have their sleep monitored with electroencephalogram (EEG) and donate their brains after they died.
Being able to compare sleep data with microscopic views of their post-mortem brain tissue was the key to answering a question that scientists have been pondering for years.
The team found 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 tired during the day because they didn’t sleep at night. It’s that the system in their brain that would keep them awake is gone.
The opposite phenomenon occurs in patients with other neurodegenerative conditions, such as progressive supranuclear palsy (PSP), who were also included in the study.
Those patients have damage to the neurons that make them feel tired, so they are unable to sleep and become sleep deprived.
The team developed the hypothesis that Alzheimer’s patients were having trouble staying awake, after discovering a set of neurons that keep us awake and that are affected in Alzheimer’s from the onset of the disease.
To determine what’s contributing to the degradation of these neurons in Alzheimer’s, the researchers looked at the brains of 33 patients with Alzheimer’s, 20 with PSP, and 32 volunteers who’d had healthy brains through the end of life.
The team measured the amounts of two proteins often associated with the neurodegenerative process—beta-amyloid and tau.
During sleep, the brain clears out the beta-amyloid that accumulates during the day. When we can’t sleep, it builds up. So, since the PSP patients never sleep, the team expected to see lots of protein in their brains.
But it turns out that they have none. These findings confirm with direct evidence that tau is a critical driver of sleep disturbances.
That idea is currently being tested in a clinical trial of patients with PSP, using a treatment that specifically targets the overactive ‘awake’ system that keeps these patients from sleeping.
This approach contrasts with the traditional trial-and-error treatment with sleep medications.
The team expects the research to lead to new ways of treating sleep disturbances driven by neurodegeneration.
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