Summary: A new study published in The Journal of Nuclear Medicine demonstrates that 213Bi-BPy targeted alpha-therapy can significantly reduce beta-amyloid plaques in the brain, offering a potential new treatment for Alzheimer’s disease.
Key Takeaways
- 213Bi-BPy targeted alpha-therapy shows potential to significantly reduce beta-amyloid plaques in the brain, offering a novel treatment option for Alzheimer’s disease.
- The therapy’s ability to bind selectively to beta-amyloid plaques and cross the blood-brain barrier demonstrates its effectiveness in targeting the root cause of Alzheimer’s disease.
- Early results suggest that this approach could slow Alzheimer’s progression and improve cognitive function, marking a potential breakthrough in Alzheimer’s treatment.
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A newly developed radionuclide therapy can precisely target and break-up beta-amyloid plaques associated with Alzheimer’s disease from the brain, representing a potential new treatment option for patients. Published in the September issue of The Journal of Nuclear Medicine, this first-of-its-kind study showed that 213Bi-BPy targeted alpha-therapy could significantly reduce the amount of beta-amyloid plaque concentration in brain tissue.
Alzheimer’s Cases to Double by 2050
Alzheimer’s disease is the sixth leading cause of death in the United States. By 2050, the number of people diagnosed with Alzheimer’s disease is expected to double. Most current treatments for Alzheimer’s disease focus on the symptoms, however, the development of therapies to treat the root cause of Alzheimer’s disease is a growing research area.
“Targeted alpha-therapy has been shown to be effective in treating metastatic cancers as it delivers tumor-localized α-particles to break-up disease-associated covalent bonds,” says Tara E. Mastren, PhD, assistant professor of nuclear engineering at the University of Utah in Salt Lake City. “Our hypothesis is that this same delivery system could be used to break up beta-amyloid plaques in the brain.”
Targeted Alpha-Therapy
In the study, researchers synthesized and radiolabeled 213Bi-BiBPy to act as a targeted delivery system for a radionuclide therapy. They evaluated its binding affinity to beta-amyloid plaques and potential to transport across the blood-brain barrier. In vitro and ex vivo preclinical studies were performed to measure the reduction of beta-amyloid concentration.
213Bi-BiBPy was shown to bind selectively to beta-amyloid plaques with high specific activity. Initial experiments also showed a stark reduction of beta-amyloid plaque when exposed to targeted alpha-therapy, up to 100 percent depending on the dose.
“Our findings are significant as they have the potential to elicit a paradigm shift in the way we treat Alzheimer’s disease,” says Mastren. “We are still in the very early stages of investigation, however if we are successful, we hope such treatments could slow down the progression of Alzheimer’s disease and potentially have a positive impact on cognitive function.”
Featured image: Amyloid beta in brain homogenate (left) treated with alpha particles emitted from [213Bi]-BiBPy (center) to achieve complete reduction of amyloid beta shown via western blot (right).
