Recent studies are showing that Alzheimer’s might be linked to more than just deteriorating brain matter and plaque. It could be a whole-body phenomenon. The findings published in Molecular Psychiatry offer hope that future drug therapies might be able to stop or slow the disease without acting directly on the brain. Instead, the drugs might be able to target areas such as the liver and kidney to flush out the toxic proteins that cause dementia before ever reaching the brain.
“Alzheimer’s disease is clearly a disease of the brain,” said Dr. Weihong Song, University of British Columbia psychiatry professor. “Our research shows that we need to pay attention to the whole body to understand where it comes from.”
Song and Yan-Jiang Wang, a neurology professor at the Third Military Medical University in Chongqing, China, demonstrated the mobility of a protein linked to Alzheimer’s disease through a technique called parabiosis. The technique involves surgically attaching two specimens together so they share the same blood supply for several months.
The scientists attached normal mice, which don’t naturally develop Alzheimer’s disease, with mice modified to carry a mutant human gene that produces elevated levels of the protein called amyloid beta. In people with Alzheimer’s disease, that protein ultimately forms clumps, or “plaque”.
The findings described the mice who had been attached to an amyloid beta inflicted counterpart ended up “contracting” the disease, all in just a few months.
Not only did the normal mice develop plaque, but also “tangle”-like pathology, which are twisted protein strands that form inside brain cells that disrupt their function to eventually kill them from the inside-out. Other signs of Alzheimer’s-like damage included brain cell degeneration, inflammation, and microbleeds. Even the ability to transmit electrical signals involved in learning and memory were impaired after a brief time being joined.
Amyloid beta is produced in other areas of the body besides the brain. It can be found in blood platelets, blood vessels, and muscles, and its forerunner protein is found in several other organs. Until these experiments, it was unclear if amyloid beta from outside the brain could contribute to Alzheimer’s disease. It appears from this study, that indeed it can.
“The blood-brain barrier weakens as we age,” says Song. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating deterioration.”
Perhaps in the near future, researchers and scientists will develop a drug that would tag the amyloid beta biochemically in such a way that the liver or kidney will be able to flush it out before generating damage.