A therapy that consists of exchanging the blood of mice that presented amyloid precursor proteins that cause Alzheimer’s disease to replace it with whole blood from healthy mice of the same genetic origin could become an innovative treatment for this devastating disease.
The results of the study that have been published in «Molecular Psychiatry» provide a «proof of concept for the use of technologies commonly used in medical practice, such as plasmapheresis or blood dialysis, to ‘clean’ the blood of Alzheimer’s patients , reducing the accumulation of toxic substances in the brain”, says Claudio Soto, from the School of MedicineMcGovern of UTHealth Houston, USA “This approach has the advantage that the disease can be treated in the circulation rather than in the brain.”
This approach has the advantage that the disease can be treated in the circulation rather than in the brain.
Previous studies by de Soto’s team have shown that misfolding, aggregation, and accumulation of amyloid beta proteins in the brain play a critical role in Alzheimer’s disease. Therefore, preventing and removing misfolded protein aggregates is considered a promising treatment for the disease.
However, the treatment of Alzheimer’s disease has been complicated for a long time, due to the difficulty of delivering therapeutic agents across the blood-brain barrier.
Thanks to their latest research, the researchers discovered that the handling of circulating components in Alzheimer’s disease could be the key to solving this problem.
“Blood vessels in the brain are classically considered the body’s most impermeable barrier,” says researcher Akihiko Urayama. “We are aware that the barrier is at the same time a very specialized interface between the brain and the systemic circulation.”
After multiple blood transfusions, the researchers discovered that the development of brain amyloid plaques in a transgenic mouse model of Alzheimer’s it was reduced by between 40% and 80%. This decrease also translated into improved spatial memory performance in aged mice with amyloid pathology, and reduced plaque growth rates over time.
Although the exact mechanism by which this blood exchange reduces amyloid pathology and improves memory is currently unknown, there are multiple possibilities. One possibility is that the reduction of amyloid beta proteins in the bloodstream may help facilitate redistribution of the peptide from the brain to the periphery.
Another theory suggests that blood exchange somehow prevents the influx of beta amyloid, or inhibits the reuptake of removed beta amyloid, among other possible explanations.
However, regardless of the mechanisms of action associated with blood exchange treatment, the study shows a new line of treatment for Alzheimer’s disease.