For years, experts thought Alzheimer’s, a progressive neurodegenerative disease, originated in the brain. After all, it’s the organ that takes the beating: Proteins build up in the brain, forming plaques or tangles that can damage cell function.
And depending on which hypothesis you’re reading up on, the critical damage that kick-starts symptoms comes from either beta-amyloid proteins, the traditional suspects, or tau proteins, a relatively new but increasingly popular pick for the potential culprits.
Recently, though, studies have come out that suggest other bodily systems, like the gut, could play a not-insignificant role in the disease’s onset. And now, a new paper published in Molecular Psychiatry, supports that nascent line of thinking by claiming that our blood could also be a player.
An international team of researchers worked with two sets of mice: One set was genetically engineered to produce high levels of a human-specific beta-amyloid and the second was normal and healthy. The group then surgically joined the healthy mice with the diseased mice, a technique called parabiosis, so that the two would share blood supplies anywhere from two months to a year.
Mice who swapped blood for at least four months developed no shortage of human-specific beta-amyloid plaques in their brains. And, in some healthy mice, brain cells involved in learning and memory were already having trouble signaling to each other at the four-month mark.
One of the paper’s authors, Weihong Song, a psychiatry professor at University of British Columbia, explains these symptoms started cropping up in the healthy mice because beta-amyloid was traveling from their diseased partner’s blood and making its way to their once-normal brains. While experts knew other parts of the body produce beta-amyloid, all this time, they largely thought the buildups we see in Alzheimer’s patients originated from the brain cells themselves. These results shine a light on the fact that the protein can make its way to the brain from other areas and have an impact on the disease’s development and progression.
This realization should help researchers keep in mind how the body as a whole impacts Alzheimer’s disease. “There is so much narrowing of focus on the brain,” Song says, “but we also have to think about other systems.”