Tsuneya Ikezu, MD, PhD, Collaborates with Industry to Study Effects of AD-associated Genetic Variants on Brain

COM-IkezuProfessor of Pharmacology & Experimental Therapeutics, and Neurology Tsuneya Ikezu, MD, PhD, has formed a research collaboration with Eisai Inc. to study the effects of Alzheimer’s disease-associated genetic variants on the behavior of brain cells, called microglia. Recent discoveries regarding the genetic underpinnings of Alzheimer’s disease (AD), suggest that microglial cells are believed to play a key role in resistance to or susceptibility in developing AD and other neurodegenerative diseases.

According to statistics from the Alzheimer’s Association, AD currently affects more than 5 million people in the U.S., and results in an estimated $259 billion cost to the nation. Over 16 million Americans are predicted to be living with Alzheimer’s by 2050, which would have an estimated $1.1 trillion cost to the U.S.

Under the two-year agreement, Ikezu will work with Eisai’s immuno-dementia discovery research team, to study the functional impact of AD-associated genetic variants on microglial biology. Ikezu’s lab has extensive experience in the cell biology of microglia, and has studied how the innate aspect of the central nervous system (CNS) influences the pathology and progression of neurodegenerative disease. He recently received the Alzheimer’s Association’s Inge Grundke-Iqbal Award for Alzheimer’s Research, based on his work on microglia and exosome-mediated tau propagation.

“Microglia are the latest brain cell types of intense investigation at both basic and translational neuroscience research levels, and their genetic association with Alzheimer’s disease is only strengthened by report after report. Development of cellular platform to study microglia biology is essential for the research community and R&D in the industry,” said Ikezu.

Eisai has experience in the AD area, having spent over 33 years working on the development of potential treatments, including Donepezil, the first compound found to show improvements on cognitive clinical scales, such as the Alzheimer’s Disease Assessment Scale cognitive subscale (ADAS-cog) and Clinician’s Interview-based Impression of Change with caregiver input (CIBIC+).

The goal of the collaboration is to understand the mechanisms underlying known genetic drivers of microglial malfunction, which are believed to play a central role in the pathogenesis of AD dementia. Utilizing information attained from the study, the parties hope to develop tools for understanding microglial biology and dissect the functional impact of microglially expressed proteins. Such discoveries may accelerate innovative therapeutic drug development for AD.