According to a recent study from UTHealth Houston, the complete exchange of blood may be a novel, disease-modifying treatment for Alzheimer's disease. This treatment successfully reduced the development of amyloid plaque in mice's brains.
This study has been published in the Journal 'Molecular Psychiatry'.
In a series of whole blood exchange procedures, a research team led by senior author Claudio Soto, PhD, professor in the Department of Neurology at McGovern Medical School at UTHealth Houston, and first author Akihiko Urayama, PhD, associate professor in the division, replaced a portion of the blood from mice exhibiting the amyloid precursor proteins that cause Alzheimer's disease with complete blood from healthy mice with the same genetic background. The study's findings were released in Molecular Psychiatry today.
According to Soto, director of the George and Cynthia Mitchell Center for Alzheimer's Disease and Related Brain Disorders and holder of the Huffington Foundation Distinguished Chair in Neurology at McGovern Medical School, "this article provides a proof-of-concept for the utilisation of technologies commonly used in medical practise, such as plasmapheresis or blood dialysis, to "clean" blood from Alzheimer's patients, reducing the buildup of toxic substances in the brain. "This strategy has the benefit that the sickness may be treated in the circulation rather than in the brain," says the author.
Soto and other UTHealth Houston scientists have previously demonstrated that the misfolding, aggregation, and accumulation of amyloid beta proteins in the brain is a key factor in Alzheimer's disease. As a result, it is thought that avoiding and eliminating misfolded protein aggregates is a possible therapy for the condition.
However, the delivery of therapeutic drugs across the blood-brain barrier has long been a challenge, making Alzheimer's disease therapy challenging. Urayama, Soto, and others found that controlling circulating components in Alzheimer's disease might be the answer to this problem through their most recent study.
According to Urayama, blood arteries in the brain are typically thought of as the body's most impermeable barrier. The barrier is simultaneously a highly specialised interface between the brain and the systemic circulation, as we are aware.
The formation of brain amyloid plaques in a transgenic mouse model of Alzheimer's disease was shown to be decreased by 40% to 80% following many blood transfusions, according to the researchers. In older animals with amyloid disease, this lowering also enhanced spatial memory ability and slowed plaque development rates.
Although the precise mechanism by which this blood exchange decreases amyloid disease and enhances memory is not yet known, there are a number of potential explanations. One theory is that reducing blood levels of amyloid beta proteins would make it easier for the peptide to be redistributed from the brain to the periphery. Another hypothesis is that blood exchange, among other possible factors, somehow limits the re-uptake of cleared amyloid beta.
However, the study demonstrates that a target for Alzheimer's disease therapy may reside in the peripheral, regardless of the mechanisms of action connected with the blood exchange treatment.