A research team led by Prof Nancy Ip of HKUST found that interleukin-33 (IL-33) ameliorates cognitive decline and Alzheimer’s disease-like pathology. The groundbreaking study has just been published in PNAS.
Defects in the removal of Aβ protein in the brain are believed to be one of the major causes underlying AD. The team at HKUST showed that the presence of IL-33 mobilized the immune cells of the brain, the microglia, to the amyloid plaques and promoted the clearance of Aβ protein. IL-33 also triggered changes in the microglia to reduce overall inflammation in the brain. Inflammation contributes to and drives the pathology of the disease.
“These exciting findings bring us one step closer to understanding the pathological process of this complex, multi-factorial disease and provide a new avenue for developing AD treatments,” said Prof Ip. “The next step will be to translate the findings from the mouse study into clinical treatments for humans.”
Amy K. Y. Fu, Kwok-Wang Hung, Michael Y. F. Yuen, Xiaopu Zhou, Deejay S. Y. Mak, Ivy C. W. Chan, Tom H. Cheung, Baorong Zhang, Wing-Yu Fu, Foo Y. Liew, and Nancy Y. Ip. (2016) IL-33 ameliorates Alzheimer’s disease-like pathology and cognitive decline. Proc Natl Acad Sci USA doi: 10.1073/pnas.1604032113.