"The main point of this study is to show the amyloid-β [from blood circulating outside of the brain] can get into the brain and deposit there and form the Alzheimer pathologies".
Besides the brain, Aβ is produced in blood platelets, blood vessels, and muscles, and its precursor protein is found in several other organs.
Now unable to remember where it left its cheese and prone to mood swings, the previously undiseased rodent suffers a number of Alzheimer's-like effects: plaques, twisted protein strands (which slowly kill brain cells from the inside out), inflammation, microbleeds. The research offers pathways to new drug therapies that could potentially stop or slow the disease without working directly on the brain.
Mice do not naturally develop Alzheimer's disease, but the researchers attached a normal mouse to a genetically modified one with mutated genes that produced high levels of a protein called amyloid-beta, prevalent in people with Alzheimer's.
Song said researchers found the normal mice eventually ended up developing the protein plaques and Alzheimer's disease-like pathologies after a year of being conjoined.
He said: "There will be amyloid protein passed between people through blood transfusions regardless of whether they have Alzheimer's, because amyloid protein can be produced outside the brain". The technique involves surgically attaching two specimens together so they share the same blood supply for several months.
After 12 months of connected blood circulation the normal mice connected had effectively "contracted" Alzheimer's disease from their genetically-modified partner.
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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.
The downside to this is, drugs that may potentially treat dementia (Alzheimer's is a form of dementia), would not work in the brain. The proteins had traveled into the brains of the normal mice and developed into plaques causing a variety of Alzheimer's-like symptoms.
"AD [Alzheimer's disease]-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice", the authors of the study detailed.
In addition, the ability to transmit electrical signals involved in learning and memory was impaired even in mice that had been joined for just four months.
He says the results show that they do.
"The blood-brain barrier weakens as we age".
Dr. Weihong Song, a UBC psychiatry professor and a Canada Research Chair in Alzheimer's Disease, says his research team focused on the amyloid-β protein, a protein of unclear function which is normally produced everywhere in the body.