NIH funds research to determine air pollution’s role in Alzheimer’s Disease

Study to utilize human-derived neurons and genomics to assess neurotoxicity of air pollution

Kitsawa Masahi
Left: Masashi Kitazawa, PhD (UCI Public Health) & right: Vivek Swarup, PhD (UCI Bio Sci)

The National Institute of Neurological Disorders and Stroke (NINDS) has awarded $2.3 million to a team of UCI researchers who are studying how air pollution drives the degeneration of neurons and how Alzheimer’s disease (AD) risk genes interact with such environmental contaminants to exacerbate its neurotoxicity. AD is the most common cause of dementia among the elderly and is an apparent public health challenge in the U.S. as well as many other countries.

Principal Investigators of the study include Masashi Kitazawa, Ph.D., associate professor of environmental and occupational health at the UCI Program in Public Health, and Vivek Swarup, Ph.D., an assistant professor of neurobiology and behavior at the UCI School of Biological Sciences. In addition, Michael Kleinman, Ph.D., adjunct professor of environmental and occupational health at the UCI Program in Public Health, and Mathew Blurton-Jones, Ph.D., professor of neurobiology and behavior at the UCI School of Biological Sciences are participating as co-investigators in the study.

Despite the extensive research effort on all aspects of AD, the exact causes of late-onset, sporadic AD remain elusive. Although genetic predispositions including known risk genes from human genetics studies are playing a prominent role in the pathogenesis and etiology of AD, recent growing bodies of evidence strongly suggest an emerging role of environmental contribution, particularly toxic constituents of air pollution including, but not limited to, particulate matter and metals, to the progression and onset of AD.

Researchers will use several innovative tools, such as a novel mouse model, human neurons, and CRISPR-based functional genomics, to carefully assess the neurotoxicity of particulate matter, its risk for developing and exacerbating AD phenotypes, and the genetic and environmental interactions. Their approach could be more clinically relevant and applied to the broader general population compared to existing findings from widely used animal models overexpressing familial AD mutations. 

“We believe that the study’s outcomes could have a large impact on the environmental health field while accelerating progress towards understanding the environmental impact on the pathogenesis of Alzheimer’s Disease,” says Kitazawa.