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Can we target Alzheimer’s at the molecular level? Dr. Tara Mastren’s research says yes—and just received $100K to prove it.


Alzheimer’s Disease affects nearly six million people in the U.S. today, a number expected to more than double by 2050. While current FDA-approved treatments can slow progression, they don’t reverse the disease—and come with serious side effects, including brain swelling. The question researchers are racing to answer is: Can we develop a safer, more effective way to break up the plaques that progress Alzheimer’s, and possibly reverse its course?

Dr. Tara Mastren is tackling this challenge head-on with a new approach: targeted alpha therapy (TAT). This method, often used in cancer treatment, delivers high-energy particles directly to harmful proteins—in this case, the amyloid beta (Aβ) aggregates that form plaques in the Alzheimer’s-affected brain. Dr. Mastren is working with University of Utah collaborators Dr. Andrew Roberts, Associate Professor of Chemistry and Dr. Donna Cross, Professor of Radiology to develop appropriate targeting compounds and study them in genetically engineering mice with Alzheimer’s.

Their research just received a major vote of confidence. The Society of Nuclear Medicine and Molecular Imaging (SNMMI) has awarded Dr. Mastren and her team $100,000 from its prestigious Mars Shot Fund, which supports bold, potentially game-changing ideas in nuclear medicine.

“We’re exploring whether we can use an alpha-emitting compound to not only break apart the protein clumps in Alzheimer’s, but also stimulate a protective immune response that reduces inflammation in the brain,” said Dr. Mastren.

Her early proof-of-concept studies have already shown promise. Lab tests demonstrated that TAT can reduce Aβ in mouse brain tissue, and a follow-up study using the compound [²¹¹At]3’-At-PIB-OH showed reduced plaque levels in genetically engineered mice with Alzheimer’s. The Mars Shot grant will fund the next stage of research, which will focus on evaluating long-term efficacy and safety of the treatment.

If successful, the implications could extend well beyond Alzheimer’s. The same strategy could potentially be applied to a host of neurodegenerative diseases caused by protein aggregation, including Parkinson’s, ALS, and Huntington’s disease.

In addition to her spearheading consistent breakthroughs in nuclear medicine, Dr. Mastren was recently promoted to Associate Professor with tenure, effective July 1, 2025—a milestone that reflects her growing leadership in nuclear medicine research.

Dr. Mastren is helping redefine what nuclear medicine can do—not just for cancer, but for brain health and beyond. We’re excited to see her work continue to grow as an Associate Professor in the Utah Nuclear Engineering Program (UNEP).

by Joe LaFata

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