New research has assessed whether ‘circulating’ amyloid beta proteins in the blood contribute to Alzheimer’s disease onset – and the answer seems to be yes.
It is well known that amyloid beta proteins, when clumped together, form toxic plaques in the brain, killing cells.
However, amyloid beta doesn’t just circulate in the brain, but also circulates in the blood stream. This new study, published in the Journal Molecular Psychiatry has used an interesting technique to find out the answer to the question of whether blood circulating amyloid beta is just as responsible for disease onset.
The technique was called Parabiosis.
What is Parabiosis?
Parabiosis is a laboratory technique where two specimens are surgically attached together (usually in mice), and the two specimens then share the same blood supply for several months.
What did they find when they did this?
The research team surgically attached mice, genetically modified to develop human forms of Alzheimer’s disease pathology such as amyloid beta, to wild type mice (i.e. controls).
After a few months, the wild type (control) mice started to develop the same Alzheimer’s disease pathology.
This is one of the first studies of its kind to suggest that amyloid beta circulating in the blood supply can actually cause Alzheimer’s disease pathology and impact negatively on brain cells.
Dr Song from the University of British Columbia and an author of the study said the blood-brain barrier weakens as we age.
“That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration,” Dr Song said.
So, while it is a bit of a strange technique, the results suggest that new treatments might need to target both Alzheimer’s disease related markers circulating in the blood supply as well as the brain.
Further research is of course needed to validate these results.
Read the full study via Molecular Psychiatry.