Being able to catch Alzheimer’s through blood transfusions and surgical equipment has long been a hotly-contested theory. Though new hesitant research does suggest that there might be some truth behind the claim.

The research from the team of scientists from the University of British Columbia in Vancouver has shown that, by connecting the blood circulation of mice, the spread of Alzheimer’s plaques can occur.

The study, led by Weihong Song, found that when researchers conjoined a healthy mouse together with a mouse that had Alzheimer’s plaques, the healthy mouse would eventually develop plaques of the beta-amyloid protein itself. This protein caused the Alzheimer plaques to form in the healthy mouse’s brain, initiating a process in which their brain tissue would start dying.

Plaques of the misfolded beta-amyloid proteins are known to accumulate in the brain of people who have the disease. It’s already well-known that misfolded proteins like beta-amyloid and other prion proteins can spread brain diseases, so the confirmation seems to prove that the disease can indeed spread.

“The protein can get into the brain from a connected mouse and cause neurodegeneration,” said Song.

As mice don’t naturally develop Alzheimer’s, the team had to put a beta-amyloid gene into healthy rodents, which enabled them to develop the brain plaques that lead to the same neurodegeneration seen in humans. By surgically attaching one mouse with the gene to a healthy mouse, the scientists were able to link them together, simulating a shared blood system.

The healthy mice began to accumulate the beta-amyloid proteins in their brains and within four months, the team found that in the regions of the brain that were key for memory and learning, they started showing devastating patterns of activity seen in Alzheimer’s.

Still, Song’s team is still wary of drawing any conclusions themselves as stitching mice together isn’t really a situation that applies at all to humans.

The hope is that this research will pave the way for the invention of new drugs, as scientists look to treatments that target the beta-amyloid protein plaques, rather than the brain.