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Disruptive Sleep and Alzheimer's Patients

Scientists are coming closer to finding out how Alzheimer’s disrupts sleep patterns, and that could eventually lead to more effective ways to improve sleep among AD patients.

People with Alzheimer’s often have poor biological rhythms that result in fragmented sleep as well as agitation in the late afternoon and early evening, a phenomenon known as “sundowning.” But it hasn’t been clear until now whether the biological clock is disrupted or destroyed altogether.

In the most recent study, researchers from Cambridge University, UK, worked with fruit flies – a key species for studying Alzheimer's. Evidence suggests that the A-beta peptide, a protein, is behind at least the initial stages of the disease in humans.

Taking a group of healthy flies and a group with A-beta peptide, the researchers studied sleep-wake patterns in the flies, and how well their biological clocks were working.

To do that, the researchers attached the protein luciferase – an enzyme that emits light – to one of the proteins that forms part of the biological clock. Because luciferase levels rise and fall during the night and day, the protein provided a way of tracing the flies' internal clock.

Damian Crowther, of Cambridge's Department of Genetics, one of the study's authors, said that the goal was to find whether the biological clock in AD patients had stopped ticking altogether or had just stopped responding.

The investigators found that diurnal patterns of the luciferase-tagged protein were the same in both healthy and diseased flies, showing that the biological clock still ticks in flies with Alzheimer's.

"Until now, the prevailing view was that Alzheimer's destroyed the biological clock," said Crowther.

"What we have shown in flies with Alzheimer's is that the clock is still ticking but is being ignored by other parts of the brain and body that govern behaviour. If we can understand this, it could help us develop new therapies to tackle sleep disturbances in people with Alzheimer's."

The findings were published in the journal Disease Models & Mechanisms.

 

 

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