Better sleep may lead to a better fight against Alzheimer’s disease

Research team at Université de Montréal offers insights that may help both detect and treat the disease among patients in the future

From left to right: Dr. Jonathan Brouillette, Ms. Audrey Hector, Dr. Valérie Mongrain

Many Canadians are having trouble getting the sleep they need to stay healthy. The Canadian 24-Hour Movement Guidelines recommend that adults, aged 18-64, get 7 to 9 hours of good quality sleep on a regular basis, with a consistent sleep and wake times for health benefits.

A recent study published by Statistics Canada found that while three-quarters of Canadian adults meet the recommendations for sleep duration, poor sleep quality and high variability in sleep times were common.

A lack of good quality sleep can affect a person’s ability to function during the day, and it may also increase the risk of developing Alzheimer’s disease (AD), a neurodegenerative condition that affects nearly 750,000 Canadians. 

With funding from CIHR, researchers at Université de Montréal are studying the potential link between sleep and AD to understand how the disease starts and progressively takes control of the brain.

Dr. Jonathan Brouillette and Dr. Valérie Mongrain, whose labs are located at the research centre of the Hôpital du Sacré-Coeur de Montréal, are examining how lack of sleep may accelerate the development of AD with a focus on the hippocampus, which is a part of the brain involved in learning, memory, and sleep. They are conducting this research with Audrey Hector, one of Dr. Brouillette’s PhD students.

Groups of amyloid beta proteins block communication among neurons and disrupt sleep

These researchers are particularly studying how amyloid beta proteins affect communication between neurons, or nerve cells. In AD, these proteins stick together and accumulate to form damaging plaques in the brain.

“We want to understand how fragments of these amyloid beta proteins called oligomers attach to neurons and interfere with intercellular communication before forming plaques,” said Dr. Mongrain, an Associate Professor at Université de Montréal and a Canada Research Chair in Molecular Sleep Physiology.

“This communication failure is harmful because it prevents healthy cells from interacting,” said Dr. Brouillette, an Associate Professor of Research in the Department of Pharmacology and Physiology at Université de Montréal. “If we can understand how these amyloid beta oligomers affect neurons and impact sleep patterns, we may eventually identify novel biomarkers and therapeutic targets that are present at the beginning of AD.”

The researchers are carrying fundamental studies to understand how amyloid beta proteins affect sleep patterns, memory, and brain activity.

Their studies have involved injecting amyloid beta proteins into the hippocampus of mice and rats and analyzing the effects through use of a variety of sophisticated technologies. These technologies include a water maze that test memory retention and the use of colorization to track the spread of the amyloid beta proteins in the brain. They also use electroencephalography (EEG) to measure changes in brain waves that impair sleep and microdialysis to detect how many amyloid beta oligomers prevent communication between neurons in brain tissue.

“We’re examining how the amyloid beta proteins affect the 24-hour cycles of lab animals,” said Ms. Hector. “We’re analyzing sleep changes and the electrical activity in their brains during sleep and studying the impact of amyloid beta proteins on the hippocampus and other parts of the brain as well as the survival of neurons.”

Their research suggests that amyloid beta oligomers increase the rate of electrical activity in the central nervous system and cause neurons in the hippocampus to become hyperactive due to blocked communication. As a result, this activity likely disrupts sleep patterns and leads to the deterioration of memory.

Sleep as a potential treatment for Alzheimer’s disease

The researchers hope that their findings will lead to collaborative studies involving human subjects.

“If other researchers are studying people in their 40s or 50s who have not been diagnosed with AD but who exhibit similar disruptions in sleep patterns, this effect on sleep could result from the amyloid pathology that we’re observing in our research,” said Ms. Hector.

“If we can find a biological marker for AD from our fundamental research,” said Dr. Brouillette, “we can share this finding with other researchers who could pursue clinical trials to determine if the marker can be used for the early detection of AD in humans.”

“I’ve always wanted to know how the brain works,” said Dr. Mongrain. “This includes understanding its communication circuits so that doctors can improve a patient’s well-being. In this case, if we can predict the onset of AD and then improve a patient’s sleep patterns through lifestyle changes, we may help prevent or slow the progression of the disease.”

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