Ken Fukuchi, MD, PhD, professor with the University of Illinois College of Medicine Peoria (UICOMP) was awarded a $2.4 million grant from the National Institutes of Health (NIH) for his Alzheimer’s research project “Role of MyD88 signaling in systemic inflammation and Alzheimer Disease.”
More than 6 million Americans currently have Alzheimer’s disease (AD), and no satisfactory treatment is available. People with AD develop two types of deposits of abnormal protein aggregates in the brain – amyloid plaques and neurofibrillary tangles. Both of these protein aggregates are posited to be toxic to brain cells (neurons). This leads to cognitive disability and dementia. Called the amyloid and tau hypothesis, this concept is currently driving Alzheimer’s research activity.
However, scientists do not know exactly how and why these abnormal protein aggregates form, particularly in the brains of AD patients. Under normal circumstances, brain immune cells, called microglia, can sense the abnormal protein aggregates and eliminate them to protect neurons from death.
Alzheimer’s researchers believe that multiple factors including genetics, lifestyle and environments are involved in the development of AD and identified factors that increase the risk of developing AD. Such AD risk factors are aging, hypertension, diabetes, obesity, high cholesterol and certain infections. Through his work studying AD, Fukuchi believes the strongest common denominator of these risk factors is chronic and systemic inflammation. He and his research team found that chronic and systemic inflammation induces abnormal activation of the microglia in the brain through a specific signaling pathway called MyD88.
With this NIH grant award, Fukuchi will test the hypothesis that chronic and systemic inflammation that accompanies AD risk factors induces microglial dysfunction, leading to accumulation of aggregated amyloid and tau proteins in the brain. The goals of this five-year project are to elucidate the molecular and cellular mechanisms underlying the AD risk factors associated with chronic and systemic inflammation and to develop new preventive and therapeutic strategies for AD.