01 July 2019

Clusterin is a disruptor of synapses

Scientists have discovered a protein that damages brain connections

"Scientific Russia"

Scientists have found out how a gene that increases the risk of Alzheimer's disease destroys brain cells, according to a press release of the Dementia study links gene with damage to brain connections.

The brain tissue of people with Alzheimer's disease has shown that a protein called clusterin accumulates in vital parts of neurons that connect cells and can damage these connections.

Scientists say that the data obtained shed light on the causes of the disease and will help speed up the search for a cure.

The study, led by Professor Tara Spears-Jones from the University of Edinburgh, focused on synapses – connections between brain cells that provide the flow of chemical and electrical signals. These signals are vital for memory formation and are key to brain health, experts say.

Researchers have shown that synapses in people who died from Alzheimer's disease contained clusters of clusterin, which could contribute to the development of dementia symptoms. These synapses also contained clusters of beta-amyloid, a destructive protein found in the brains of people with Alzheimer's disease.

People with a common risk gene called apolipoprotein E4 had more clusters of clusterin and beta-amyloid in their synapses than people with Alzheimer's disease without the risk gene. Those without dementia symptoms had even fewer disruptive proteins in their synapses.

Clusterin.jpg

A drawing from an article by Jackson et al. Clusterin accumulates in synapses in Alzheimer's disease and is increased in apolipoprotein E4 carriers, published in the journal Brain Communications – VM.

The discovery was made using powerful technology that allowed scientists to view detailed images of more than a million synapses. Individual synapses are about 5,000 times smaller than the thickness of a sheet of paper.

The loss of synapses in Alzheimer's disease has been established previously, but the lump of damaging proteins in synapses has so far been unknown due to difficulties in studying them due to their tiny size.

Alzheimer's disease is the most common form of dementia, affecting about 500,000 people in the UK. It can cause serious memory loss, and there is no cure for it yet.

Professor Spiers-Jones, head of the program at the Dementia Research Institute in the UK at the University of Edinburgh, said: "We have identified a new player in a variety of proteins that damage synapses in Alzheimer's disease. Synapses are essential for thinking and memory, and preventing their damage is a promising goal to help prevent or eliminate the symptoms of dementia. This work gives us a new way to develop effective treatments."

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