Researchers in Scotland are trying to unravel the complex relationship between sleep, dementia, and the brain's immune cells in a new study into Alzheimer's disease.
The 18-month pilot project, funded by a £70,000 investment from Alzheimer's Research UK, will be carried out at Strathclyde University.
Dr Shuzo Sakata, an expert in brain function and pathology, will lead the project looking to better understand the link between sleep and Alzheimer’s disease, in the hope of finding new ways to prevent the disease.
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Research has shown that changes in sleep patterns are common in people with dementia, even in its early stages.
However, the connection between sleep and dementia is still a mystery.
Dr Sakata will examine how sleep disruption affects the brain’s immune cells - known as microglia.
Microglia protect the brain by removing debris, which includes the harmful protein amyloid which builds up in Alzheimer’s disease.
During sleep, microglia in a healthy brain extend their arms and increase their levels of calcium.
When there is a lack of sleep, however, the microglia shrink their arms and become a rounded, amoeba-like shape.
How amyloid is linked to these changes in calcium is unknown.
Dr Sakata hopes that the research will eventually extend to studying the brains of human patients, but admits that this "could be a long way off".
For now, he will use advanced imaging techniques to see inside the immune cells at multiple regions of the brain in mice models of Alzheimer's.
This will enable researchers to evaluate how amyloid affects calcium levels in microglia in sleeping and waking states, and how sleep deprivation affects these calcium levels.
Dr Sakata said the project will be the first to "bridge the gap" between sleep, microglia, and dementia onset, which have tended to be studied separately.
He said: "People have looked at the relationship between Alzheimer's and sleep, and for Alzheimer's and microglia there are a lot of studies.
"There are also some imaging research into the relationship between sleep and microglia in healthy people.
"But no one has looked at these three components together - and, if I'm lucky, I might be able to find something that can lead to some new treatment."
He added that there seems to be a "bi-directional" relationship between sleep and dementia, in that the build-up of amyloid plaques in the brain leads to abnormal sleep patterns which "stimulates disease progression", but at the same time disrupted sleep can potentially fuel the build up of amyloid deposits.
"That's still a hypothesis, but we want to elucidate how microglia contribute to these bidirectional interactions," said Dr Sakata.
The project is one of two new studies in Scotland funded by Alzheimer's Disease UK in its latest £4 million research investment.
In addition, the charity has allocated £30,000 to a project at Edinburgh University investigating how the blood-brain barrier becomes damaged by the diseases which cause dementia.
The study will be led by Dr Paula Beltran-Lobo, who said she was excited to be relocating from London to Scotland to pursue her work - describing it as a "centre of excellence" for dementia research.
Dr Beltran-Lobo will be focusing on star-shaped cells called astrocytes which act as bridges, linking neurons in the brain to the vascular cells in the blood vessels.
The blood-brain barrier is a membrane which controls the movement of molecules, such as nutrients, from the bloodstream into the brain.
It is known that when a protein called tau accumulates in astrocytes during the onset of diseases such as Alzheimer's and Frontotemporal dementia, it can disrupt their function and cause the blood-brain barrier to become leaky.
"That happens early on in disease and it has devastating consequences for the neurons because they do not have enough nutrients, or some of the build ups in the brain cannot be cleared out," said Dr Beltran-Lobo.
Little is known about how tau protein builds up in astrocytes during disease, or how it affects the cell’s role in keeping the blood brain barrier healthy.
By using brains donated by people who had high levels of tau protein when they died, Dr Beltran-Lobo hopes to gain a better understanding into how tau disrupts the blood brain barrier.
Dr Beltran-Lobo said: "Most of the research has always been focused on what is happening to the neurons, and we are only starting to look at what happens to the support system around neurons.
"We are at an early stage and these diseases are very complex, but if we can prevent these damaging changes happening in the astrocytes we might be able to develop treatments which target the disease in the earlier stages.
"And because we are looking at a treatment that we could administer through the bloodstream, it might be easier than developing treatments that target the brain directly."
Dr Julia Dudley, head of strategic programmes at Alzheimer’s Research UK, added: “In the UK alone, nearly one million people are living with dementia.
"So there’s never been a more pressing need to prevent or treat the diseases that cause this devastating condition.
“Alzheimer’s Research UK is proud to support research that’s gaining a greater understanding of how these diseases develop in the brain which could lead to the breakthroughs that people with dementia deserve and need.
“It’s essential that we keep investing in studies like these to accelerate progress towards a cure, and to end the fear, harm and heartbreak from dementia.”
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