Looking for a bullseye in our genes to stop Alzheimer’s Disease progression

National Institute of Aging awards UCI researchers a grant to investigate the role of microglia in Alzheimer’s Disease

Alzheimer

The National Institute of Aging (NIA) awarded co-investigators Masashi Kitazawa, PhD, associate professor of environmental and occupational health at the UCI Program in Public Health, and Mathew Blurton-Jones, PhD, professor and director of UCI Induced Pluripotent Stem Cell Core and Vivek Swarup, PhD, assistant professor of neurobiology and behavior both from the UCI School of Biological Sciences, a three-year grant to prove a specific gene pathway is viable in detecting the onset of biological symptoms from Alzheimer’s Disease (AD). 

As a neurodegenerative disease with an elusive cause, Alzheimer’s disease continues to baffle researchers and clinicians who dedicate their careers in search of answers. On the basic science side of the battle to find a cure, there is strong evidence that shows certain gene pathways are connected to AD, which is promising for the development of targeted therapeutic drugs. For example, the gene called spleen tyrosine kinase (SYK) is well known for its ability to support the immune system when it becomes inflamed from disease. Evidence shows that SYK controls the activation pattern of microglia, which are cells that are important for coordinating the immune system’s resources during disease-associated neuroinflammation. 

There is an opportunity here to discover how critical the role SYK plays in AD progression.”

– Masashi Kitazawa, PhD

The UCI Public Health-led project aims to uncover the relationships that microglia have between cell-to-cell communication as it relates to activating AD symptoms. Using mouse models, Kitazawa and team aim to prove whether and how SYK activation and activated microglia contribute to the disease progression in AD. 

“There is an opportunity here to discover how critical the role SYK plays in AD progression,” says Kitazawa. “The study findings can potentially be used in targeted therapeutic treatment to stop the development of hallmarks of AD, such as beta-amyloid plaque build up, neuronal loss, neuroinflammation, and more.”