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Research finds possible mechanism between sleep and Alzheimer’s disease

Monday, 26 February 2018

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Edith Cowan University (ECU) research has found individuals with particular genetic variations in Aquaporin-4 (AQP4) proteins reported poorer sleep and presented with a build-up of beta-amyloid in the brain – the main component of amyloid plaques found in the brains of Alzheimer’s disease patients.

The study was led by Associate Professor Simon Laws and Dr Stephanie Rainey-Smith from ECU’s Centre of Excellence for Alzheimer’s Disease Research and Care.

They focussed on AQP4 due to its role in our brain’s night-time ‘housekeeping’ system.

“Previously, it was thought that sleep problems were simply a characteristic of Alzheimer’s disease, but more recent studies have shown that a bidirectional relationship exists, with poor sleep also contributing to higher amyloid levels,” Associate Professor Laws said.

One suggested mechanism the brain uses to remove beta-amyloid is the glymphatic system, which ‘flushes out’ toxins during sleep.

Associate Professor Laws, who leads the Collaborative Genomics group in ECU’s School of Medical and Health Science, said a key component of this system is AQP4, which is a water-channel protein that acts like tiny drains through which toxins are flushed.

“For the first time, we’ve found that people with genetic variants in AQP4 who also have problems getting to sleep and sleep for shorter periods have high levels of beta-amyloid in the brain,” Associate Professor Laws said.

“This adds strong evidence to the idea that the glymphatic system is vital, and suggests genetic variants in AQP4 may lead to a poorly functioning glymphatic system.”

Improving the system

Good sleep is vital, as the glymphatic system shuts down during waking hours.

As such, poor sleep or other factors that result in impaired functioning allow beta-amyloid to build up in the brain over time.

“In some individuals, their glymphatic system may function perfectly well on six or eight hours sleep, but this study suggests that individuals with a genetic variation might need more sleep,” Associate Professor Laws said.

While more research is required, these new findings could lead to individualised treatments for people with poor sleep quality.

The challenge will be to help people sleep longer or better, which could then compensate for a glymphatic system that functions poorly due to genetic variation.

“Approaches that may help achieve this could include modifying a person’s sleeping environment, such that noise and light is kept to a minimum,” Associate Professor Laws said.

The study ‘Genetic variation in Aquaporin-4 moderates the relationship between sleep and brain Aβ-amyloid burden’ is published in Translational Psychiatry.

Media Contact: Rob Payne, Communications Coordinator

(08) 6304 2381 / r.payne@ecu.edu.au

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