A new study from researchers at the University of British Columbia finds that a protein said to be responsible for the onset of Alzheimer’s could be originating in other organs of the body such as the kidneys or liver, meaning that the neurodegenerative disease should no longer be considered simply a brain disease but one potentially impacted by breakdowns in other regions of the body, as well.
The typical explanation for the cause of Alzheimer’s starts by saying that the disease and its symptoms are a result of brain cell death, itself brought on by a protein called beta-amyloid, which research shows can interfere with the communication between brain cells and, as a result, hasten their demise.
And scientists have long assumed that the source of the offending beta-amyloid came from brain tissue itself, which is capable of generating the protein. But other bodily systems make and circulate beta-amyloid, too, as it’s found in blood platelets, blood vessels and muscles and has a precursor protein produced in other organs, as well. All of which is to say that while it’s clear that Alzheimer’s is first and foremost a brain disease, whether the source of the problem begins in the brain itself or somewhere else in the body was still an open question — until now.
The collaborative study by researchers at UBC and Third Military Medical University in Chongqing, China, tested the theory by surgically linking mice together in groups of two, with one “normal” mouse attached to another that had been genetically modified to produce higher-than-normal levels of amyloid-beta. As the two mice shared the same circulatory system, the normal mouse was exposed to the extra amyloid-beta and, over time, was found to develop protein plaques and twisted strands of protein in the brain, both of which are characteristic of Alzheimer’s-like neural damage.
The results show that the amyloid-beta causing Alzheimer’s could be originating in other regions of the body, say the study’s authors. “To the best of our knowledge, our study is the first to reveal that blood-derived amyloid-beta can enter the brain, form the amyloid-beta-related pathologies and induce functional deficits of neurons,” say the authors.
The finding is substantial, as the previous assumption was that the blood-brain barrier — that membrane which keeps some of the blood’s compounds from passing through to the brain — would keep amyloid-beta from the rest of the body from entering brain tissue.
“The blood-brain barrier weakens as we age,” says study co-author Dr. Weihong Song, Canada Research Chair in Alzheimer’s Disease at UBC in a press release. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”
“Alzheimer’s disease is clearly a disease of the brain, but we need to pay attention to the whole body to understand where it comes from, and how to stop it,” he says.
The new research is published in the journal Molecular Psychiatry.