It has been long assumed that Alzheimer’s disease develops as a result of accumulation of two abnormal proteins called plaques and tangles in the brain, which kill brain cells. But a new study by researchers from the University of British Columbia and researchers in China indicates that this neurodegenerative disease could originate in parts of a body other than the brain.

“Alzheimer’s disease is clearly a disease of the brain, but our research shows that we need to pay attention to the whole body to understand where it comes from, and how to stop it,” says Dr. Weihong Song, UBC psychiatry professor in a news release.

In the study, Dr. Weihong Song and his colleagues carried out a procedure called parabiosis on mice. In case you’re not familiar with the term, parabiosis – it is a technique in which two specimens (in this case, mice) are surgically attached together to study the effects of one on the other. So, researchers attached normal mice, which do not have Alzheimer’s disease, to mice genetically modified to carry a mutant human gene that produces high levels of the protein called amyloid beta.

After a year of connected blood circulation, they found that the normal mice attached to genetically modified partners contracted Alzheimer’s disease. This means that the amyloid beta traveled from the genetically-modified mice to the brains of the normal mice, where it accumulated and began to inflict damage. They also found that the non-modified mice developed plaques, and “tangle”- like pathology from inside brain cells. Other signs of Alzheimer’s such as brain cell degeneration, inflammation, microbleeds  and even an impaired ability to transmit electrical signals involved in learning and memory, were also seen.

Amyloid beta is produced anywhere in the body – in blood platelets, blood vessels and muscles, and its precursor protein is found in several other organs. Previously, researchers weren’t sure if amyloid beta from outside the brain could contribute to Alzheimer’s disease. But, this new study shows it can indeed contribute to the disease.

“The blood-brain barrier weakens as we age,” Song says. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”

The study offers hope that future drug therapies might be able to stop or slow the disease without working directly on the brain. Instead, such drugs could be developed to target the kidney or liver and flush out toxic amyloid-beta proteins from the body before it can reach the brain.

The study titled “Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies” has been published in the journal Molecular Psychiatry.

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