Interleukin17A Promotes Postoperative Cognitive Dysfunction by Triggering β-Amyloid Accumulation via the Transforming Growth Factor-β (TGFβ)/Smad Signaling Pathway - Tian, Ayong; Ma, Hong; Zhang, Rongwei; Tan, Wenfei; Wang, Xiaolong; Wu, Binyang; Wang, Jun; Wan, Chengfu (PloS one, 2015)
Keywords: Accumulation; Activation; Alzheimer's disease; Amyloid beta-Peptides - metabolism; Amyloid beta-Protein Precursor - metabolism; Anesthesiology; Animal cognition; Animals; Antibodies, Monoclonal - administration & dosage; Antibodies, Monoclonal - pharmacology; Apoptosis; Astrocytes; Astrocytes - metabolism; Biomarkers; Brain research; Cognition Disorders - drug therapy; Cognition Disorders - etiology; Cognition Disorders - metabolism; Cognitive ability; Cytokines; Cytokines - metabolism; Disease Models, Animal; Gene expression; Geriatrics; Growth factors; Hepatectomy; Hepatectomy - adverse effects; Hippocampus; Hippocampus - metabolism; Hippocampus - pathology; Hospitals; Immunoglobulins; Inflammation; Interleukin 1; Interleukin-17 - antagonists & inhibitors; Interleukin-17 - metabolism; Laboratory animals; Male; Maze Learning; Memory, Short-Term; Mice; Monoclonal antibodies; Nervous system; Older people; Pathogenesis; Peptides; Phosphorylation; Postoperative Complications; Ribonucleic acid; RNA; Rodents; Signal Transduction; Signaling; siRNA; Smad protein; Smad Proteins - metabolism; Smad3 protein; Spatial Memory; Surgery; Transforming growth factor; Transforming Growth Factor beta - metabolism; Transforming growth factor-b; Tumor necrosis factor-TNF; β-Amyloid; United States--US; China