Poor sleep increases risk of Alzheimer's disease

Pearl Mccarthy
January 27, 2019

There is no cure for the disease as of yet.

Researchers at Washington University School of Medicine in St Louis found sleep deprivation increased levels of the protein tau in the brains of humans and mice. "He points out that while most of the data presented in the Cortexyme study supported their hypothesis, gingipains weren't found in all of the Alzheimer's-affected brains, 'so whilst it may be a cause, the data don't exactly support it being the only cause".

A large-scale clinical trial that will involve giving the drug to patients with mild to moderate Alzheimer's is planned for later this year. Lack of sleep alone is indicated in the findings to help drive the disease, and suggests good sleep habits may help to preserve brain health.

'This isn't just about teeth and gums.

Where did the story come from?

"Despite significant funding and the best efforts of academic, industry, and advocacy communities, clinical progress against Alzheimer's has been frustratingly slow", said Casey Lynch, Cortexyme's co-founder, chief executive officer, and an author on the Science Advances paper. The study was funded by Cortexyme, which was founded by some of the researchers involved in the study.

What kind of research was this?

The researchers of this new study say one explanation for the link is that bacteria from gum disease may access the brain by infecting immune system cells or spreading through cranial nerves passing through the head and jaw. These types of experiments are useful in early studies exploring the disease process. "Human CSF tau also increased over 50% during SD".

Ten-year-old's science project questions Tom Brady's legacy
The rational behind the accusation was that deflated footballs are easier to hold onto and travel farther when thrown. He included results of an experiment he did with his mother and sister using footballs of varying inflation.

What did the research involve?

So the authors of the new investigation saying they were "serious indications of the origin of disease from bacteria of the mouth Porphyromonas gingivalis".

In addition, the team identified toxic enzymes called gingipains secreted by the bacteria in the brains of Alzheimer's patients, which correlated with two separate markers of the disease: the tau protein, and a protein tag called ubiquitin. Targeting gingipains likely works by cutting off nutrients and other molecules that the enzyme supplies to the bacteria, Dominy says.

What were the basic results?

The most toxic enzymes were found in those with the worst cognitive decline - these samples also had more amyloid and tau protein accumulations. They said the concentration of gingipains in brain tissue was "significantly higher" in brain samples from people with Alzheimer's disease.

The team even managed to find a way to kill P. gingivalis in the brains of mice. But he stressed this won't prevent the brain from becoming infected by P. gingivalis. Giving some of these to mice reduced their infections, halted amyloid production, lowered brain inflammation and even rescued damaged neurons.

How did the researchers interpret the results?

This is not the first time that the bacteria have been linked to Alzheimer's but in their study, the researchers further investigated how it plays a role in the development of the disease.

Traditional broad-spectrum antibiotics would probably be ineffective against P. gingivalis in the brain, according to the research. However, the mechanisms around the development of Alzheimer's disease are complex. Clumps of a brain protein known as amyloid plaques are a hallmark sign of the disease. But it only shows an association, it still doesn't prove a causal link. People with Parkinson's-like those with Alzheimer's-often have sleep problems. Healthy individuals could also show P. gingivalis DNA in their CSF.

Staying up made people cranky and stressed; while it is hard to judge mouse moods they also rebounded by getting more sleep later on.

Other reports by

Discuss This Article

FOLLOW OUR NEWSPAPER