Protection of TGF-β1 against Neuroinflammation and Neurodegeneration in Aβ1–42-Induced Alzheimer’s Disease Model Rats

• Published in: PloS one Vol. 10; no. 2; p. e0116549
• Main Authors: Chen, Jia-Hui, Ke, Kai-Fu, Lu, Jian-Hua, Qiu, Yi-Hua, Peng, Yu-Ping
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 06.02.2015; Public Library of Science (PLoS)
• Subjects: Administration, Intranasal; Alzheimer Disease - chemically induced; Alzheimer Disease - drug therapy; Alzheimer Disease - pathology; Alzheimer's disease; Amyloid; Amyloid beta-Peptides - toxicity; Animals; Anti-Inflammatory Agents - administration & dosage; Anti-Inflammatory Agents - therapeutic use; Apoptosis; Blood-brain barrier; Brain; Brain-derived neurotrophic factor; CD4 antigen; Cerebrospinal fluid; Cytokines; Cytokines - metabolism; Disease; Disease Models, Animal; Glial cell line-derived neurotrophic factor; Hippocampus; Hypothalamus; Hypothalamus - metabolism; Immunosuppression; Inflammation; Inflammation - prevention & control; Injection; Injections; Insulin-like growth factor I; Interleukin 10; Interleukin 17; Interleukin 2; Interleukin 22; Laboratory animals; Lymphocytes; Lymphocytes T; Medicine; Nerve Degeneration - pathology; Nerve Degeneration - prevention & control; Neurodegeneration; Neurogenesis; Neuroglia - metabolism; Neuroglia - pathology; Neuronal-glial interactions; Neuroprotection; Neuroprotective Agents - administration & dosage; Neuroprotective Agents - therapeutic use; Neurotoxicity; Neurotrophic factors; Nitric-oxide synthase; Pathogenesis; Pathology; Peptide Fragments - toxicity; Physiology; Rats; Rats, Sprague-Dawley; Rodents; Transforming Growth Factor beta1 - administration & dosage; Transforming Growth Factor beta1 - therapeutic use; Transforming growth factor-a; Transforming growth factor-b1; γ-Interferon; United States > US; China

Neuroinflammation has been reported to be associated with Alzheimer's disease (AD) pathogenesis. Neuroinflammation is generally considered as an outcome of glial activation; however, we recently demonstrated that T helper (Th)17 cells, a subpopulation of proinflammatory CD4+ T cells, are also i...