title: The dual roles of cytokines in Alzheimer's disease: update on interleukins, TNF-α, TGF-β and IFN-γ.
abstract: Alzheimer's disease (AD) is one of the most common neurodegenerative disorders in the elderly. Although the mechanisms underlying AD neurodegeneration are not fully understood, it is well recognized that inflammation plays a crucial role in the initiation and/or deterioration of AD neurodegeneration. Increasing evidence suggests that different cytokines, including interleukins, TNF-α, TGF-β and IFN-γ, are actively participated in AD pathogenesis and may serve as diagnostic or therapeutic targets for AD neurodegeneration. Here, we review the progress in understanding the important role that these cytokines or neuroinflammation has played in AD etiology and pathogenesis.
authors.affiliation: Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030 China.
authors.forename: Cong
authors.initials: C
authors.lastname: Zheng
authors.affiliation: Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030 China.
authors.forename: Xin-Wen
authors.initials: XW
authors.lastname: Zhou
authors.affiliation: Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030 China ; Co-innovation Center of Neuroregeneration, Nantong, 226000 China.
authors.forename: Jian-Zhi
authors.initials: JZ
authors.lastname: Wang
keywords: Alzheimer’s disease; Cytokines; IFN-γ; Interleukins; TGF-β; TNF-α