Sections
Log in
Top News
U.S. News World News Featured Voices
Odd News
Entertainment
Movies Music TV
Sports
Soccer NFL NBA MLB NHL Golf Horse Racing Tennis Col. Football Col. Basketball
Photos
News Entertainment Sports Features Archives
More...
Defense Featured Science Health Archive Almanac
About Feedback
About Feedback
Search
Health News
Feb. 5, 2019 / 4:30 PM

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

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.

"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.

RELATED Researchers find dementia patients have different gut bacteria

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

"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.

RELATED Study: Women's brains have more Alzheimer's-causing proteins than men

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.

RELATED Scientists may be able to restore Alzheimer's disease memory loss

  • Topics
  • Alzheimer's Disease
Follow us on Facebook, Twitter and Instagram for more UPI news and photos.

Trending Stories

Electric bikes could improve brain function in older people
Weight-loss surgery could benefit sex life, study says
CDC warns of severe flu strain 'wave'
New recommendation could cut costly UTI tests in half, study says
Google offers drug disposal site map on Google Maps

Photo Gallery

 
The 1975, Dua Lipa walk Brit Awards red carpet

Latest News

Charges dropped against Kansas waterpark officials
Botswana officials endorse lifting elephant hunting ban
Four Venezuelan troops defect amid blockade of aid
Tainted booze in India kills 85 people, sickens hundreds
Pentagon to send another 1,000 troops to Mexican border
 
Back to Article
/
Back to top
About UPI Contact Feedback Advertisements Submit News Tips
Copyright © 2019 United Press International, Inc. All Rights Reserved.
Terms of UsePrivacy Policy