New research at Temple University’s Lewis Katz School of Medicine revealed significant discoveries in the study—and possibly the treatment—of Alzheimer’s disease.

A team of researchers led by Domenico Praticò, a professor in the Center for Translational Medicine who specializes in the pharmacology of neurodegenerative diseases, showed unequivocally that glucose deprivation in the brain induces the formation of toxic tau fibrils, which triggers the onset of cognitive decline and memory impairment.

The same study was also the first to identify a protein called p38 as causing the negative effects of Alzheimer’s, making it a potential alternative drug target for treatment of the disease. The protein is activated in response to glucose deprivation, the study showed, possibly as a defense mechanism.

“There is now a lot of evidence to suggest that p38 is involved in the development of Alzheimer’s disease,” Praticò said.

He said the next step in his team’s research is to inhibit the p38 protein to determine whether memory impairments can be alleviated, despite glucose deprivation. The study was published Jan. 31 in the journal Translational Psychiatry.

“It is an exciting avenue of research,” Praticò said. “A drug targeting this protein could bring big benefits for patients.”

Read more about the study.
—Kara Rogers