New research aims to apply targeted therapy techniques inspired by cancer treatments to people with Alzheimer’s.
Researchers have long struggled to slow the buildup of amyloid beta plaques, harmful clumps of proteins that exacerbate the disease by damaging brain cells and causing memory loss.
University of Utah researchers, however, have developed a groundbreaking approach to tackle these plaques and possibly slow this devastating neurodegenerative disease.
Inspired by targeted cancer treatment methods, their technique uses a form radiation known as alpha particles to break down chemical bonds in amyloid beta plaques. Targeted alpha therapy (TAT) delivers these particles directly to the harmful plaques on the brain while aiming to minimise damage to healthy tissues.
Aidan Bender, a former graduate student in the college’s Utah Nuclear Engineering Program, led the research, published in the Journal of Nuclear Medicine.
The Utah researchers turned to theoretical nuclear medicine in search of answers. They started by developing a chemical compound, called BiBPy, that can latch onto to the harmful amyloid beta plaques.
They attached a small amount of a radioactive isotope, bismuth-213, enabling the compound to emit alpha particles. This new compound, [213Bi]-BiBPy, was applied to the brain tissue of mice that were genetically modified to develop amyloid plaques similar to those in Alzheimer’s patients.
The compound, when combined with bismuth-213, demonstrated properties that made it effective at binding to the mice’s amyloid plaques.
Measured using two types of tests for the presence of amyloid beta, the treated brain tissues showed a significant reduction in amyloid beta concentration. These results suggest that the compound may be effectively applied as a potential TAT treatment for Alzheimer’s and other neurodegenerative diseases, paving the way for further tests in live animals and eventually in humans.
