United States: Although the underlying mechanisms remain largely unknown, new detailed research from the Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital claim that TYK2 is one of the primary drivers of toxic tau deposition, responsible for the spread of the disease in Alzheimer’s patients. Recent research in Nature Neuroscience pointed to a partial inhibition of TYK2 that would decrease tau levels and their toxicity, and thus delay further disease progression, as reported by scitechdaily.com.
The Link Between TYK2 and Tau in Alzheimer’s
Studying under Dr. Huda Zoghbi, Dr. Ji-Yoen Kim uncovered that TYK2 handles the phosphorylation of tau on a particular particle called Tyrosine 29. This alteration interferes with autophagy, a process that is crucial for the brain to dispose of toxic molecules and proteins, such as tau in neurons, a hallmark of Alzheimer’s and other neurological diseases are formed. The results represent the first proof that TYK2 contributes to tau-mediated neurodegeneration in vitro in human cells and in vivo mouse models.
MUCAC: A Potential New Therapeutic Strategy
The team used two mouse models of Alzheimer’s disease and examined that reducing TYK2 function should be only partially Therapeutic target TYK2 was identified. “Nonetheless, our data suggest that TYK2 inhibition may contribute to the reduction of tau aggregation and toxicity: further research is required,” Dr. Kim explained.
Opportunities and Strategies of TYK2 Inhibitors
Several TYK2 inhibitors exist today, some of which have been even tried on humans in relation to other diseases, suggesting that other therapeutic candidates for Alzheimer’s exist. “We are hopeful about these inhibitors’ potential to one day help bring down tau levels in the brain and therefore offer a new form of treatment for Alzheimer’s and other dementias,” Dr. Zoghbi said, as reported by scitechdaily.com.