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Blood protein contributes to memory loss in Alzheimer's disease, study says

By
Tauren Dyson
When fibrinogen leaks into the brain it activates and reprograms immune cells to sever neuron-to-neuron synapses, leading to memory loss. Photo by Riff/Shutterstock
When fibrinogen leaks into the brain it activates and reprograms immune cells to sever neuron-to-neuron synapses, leading to memory loss. Photo by Riff/Shutterstock

Feb. 5 (UPI) -- A protein found in blood could be the key to identifying the cause of Alzheimer's disease, a new study says.

When fibrinogen leaks into the brain they activate and program immune cells that severe neuron-to-neuron synapses, leading to memory loss, according to a study published Tuesday in Neuron. Those synapses are important for neurons to communicate with one another.

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"We found that blood leaks in the brain can cause the elimination of neuronal connections that are important for memory functions," Katerina Akassoglou, a professor of neurology at University of California at San Francisco and study senior investigator, said in a news release. "This could change the way we think about the cause and possible cure of cognitive decline in Alzheimer's disease and other neurological diseases."

The destruction of these synapses is associated with Alzheimer's disease and other dementias. During an experiment with mice, the researchers were able to stop fibrinogen from activating the brain's immune cells in the first place, keeping their memories intact.

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This discovery takes a detour from past research that suggests tau buildup in the brain causes Alzheimer's disease.

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"Traditionally, the build-up of amyloid plaques in the brain has been seen as the root of memory loss and cognitive decline in Alzheimer's disease," said Mario Merlini, a staff research scientist in Akassoglou's laboratory at Gladstone Institutes and study first author of the study. "Our work identifies an alternative culprit that could be responsible for the destruction of synapses."

In past research, researchers developed an antibody that blocks the ability of fibrinogen to comingle with the brain's immune cells.

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Now they want to use the current study's findings to help make breakthroughs in treating other conditions.

"These exciting findings greatly advance our understanding of the contributions that vascular pathology and brain inflammation make to the progression of Alzheimer's disease," said Lennart Mucke, director of the Gladstone Institute and study co-author.

"The mechanisms our study identified may also be at work in a range of other diseases that combine leaks in the blood-brain barrier with neurological decline, including multiple sclerosis, traumatic brain injury and chronic traumatic encephalopathy. It has far-reaching therapeutic implications," Mucke said.

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