The two solidifying instigators of Alzheimer -disease (AD)—amyloid beta and the tau protein—have long been the topic of study for AD researchers. Amyloid beta contributes to AD by solidifying into toxic plaques that accumulate in the extracellular spaces of nerve tissue and the tau protein will tangle in the bodies of neurons affecting their function. These plaques and tangles are the hallmarks of AD and as a result studies are always looking for initiating drug development that targets these hallmarks.
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Previous studies involving therapeutic development for AD specifically for targeting the hallmarks has often faced failure and the challenge to reverse cognitive decline as result of the disease remains at the forefront of research. Now, at the Arizona Center for Drug Discovery based at the UA College of Pharmacy, researchers have examined a molecule drug called ‘DYR219’ as a possible therapeutic for AD. DYR219 is believed to be unique in its ability to not target the hallmarks of AD but instead acts on the pathways that leads to these hallmarks. In other words, the drug acts as a prevention instead of a treatment.
“If you can block that process early, you can delay the downstream aggregation and formation of the pathologies,” says Travis Dunckley, a researcher at the ASU-Banner Neurodegenerative Disease Research Center.
Findings of the study were published in the journal Molecular Neurobiology and describes how the inhibitive effects of DYR219, or a similar drug, can eventually place a stop to AD development. By preventing or delaying the development of AD pathologies, DYR219 or a similar drug may halt the progression of Alzheimer’s in its tracks, before it damages the brain beyond repair.
“We showed a robust and significant delay in the onset of amyloid and tau pathology,” Dunckley says. “The reason I’m excited about this, especially in the face of a lot of the recent high profile clinical trial failures, is that this is really a different approach to treating the disease.”
Essentially, the drug works as a preventive measure by inhibiting a particular neuroactive enzyme called DYRK1 that holds crucial role in plaque and tangle formation in AD.
DYR219 is a powerful new drug developed to inhibit a kinase known as DYRK1. The inhibition targets leading pathologies of with Alzheimer's disease—plaques, (caused by the protein amyloid beta) and tangles, (caused by the tau protein). The drug can open new doors to preventing cognitive decline. Credit: Arizona State University, Graphic by Shireen Dooling
