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Crosstalk Signaling between IFN-γ and TGF-β in Microglia Restores the Defective β-amyloid Clearance Pathway in Aging Mice with Alzheimer's Disease
Biomed Sci Letters 2018;24:305-310
Published online December 31, 2018;  https://doi.org/10.15616/BSL.2018.24.4.305
© 2018 The Korean Society For Biomedical Laboratory Sciences.

Go-Eun Choi†,*

Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, Busan 46252, Korea
Correspondence to: *Professor.
Go-Eun Choi. Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, Busan 46252, Korea.
Tel: +82-51-510-0563, Fax: +82-51-510-0568, e-mail: gechoi@cup.ac.kr
Received October 24, 2018; Accepted November 15, 2018.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
 Abstract
Microglia are emerging as critical regulators of innate immune responses in AD and other neurodegenerative disorders, highlighting the importance of understanding their molecular and cellular mechanisms. We attempted to determine the role of crosstalk signaling between IFN-γ and TGF-β in Aβ clearance by microglia cells. We used in vitro and in vivo mouse models that recapitulated acute and chronic aspects of microglial responses to Aβ peptides. We showed that crosstalk signaling between TGF-β and Smad2 was an important mediator of neuro-inflammation. These findings suggest that microglial TGF-β activity enhances the pathological progression to AD. As TGF-β displays broad regulatory effects on beneficial microglial functions, the activation of inflammatory crosstalk signaling between TGF-β and Smad2 may be a promising strategy to restore microglial functions, halt the progression of Aβ-driven pathology, and prevent AD development.
Keywords : Alzheimer's disease, Microglia, IFN-γ, TGF-β, APPswe transgenic mice