Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease.
By Wen-Ying Wang, M. Tan, Jin-Tai Yu, L. Tan. Annals of Translational Medicine, 2015
1,213 citations recorded by the source corpus.
Subfields: Biological Psychiatry, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/a16ecd9ac849d64761a4ddd331781083f47d7d2a
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Citations in the corpus
- ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020, background): “Microglial NFκB is a dimer of p50 (NFκB1) and p65 (Rel-A) [138,139] and is sequestered in the cytoplasm by inhibitor of κB (IκB).”
- iPSC-derived human microglia-like cells to study neurological diseases (2017, neutral): “To this end, we measured cytokine/chemokine secretion by iMGLs stimulated by Lipopolysaccharide (LPS), and by IL-1β and IFNγ, two cytokines that are elevated in AD patients and mouse models (Abbas et al., 2002, Blum-Degen et al., 1995, Patel et al., 2005, Wang et al., 2015).”
- Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications (2017, background): “It is becoming increasingly evident that prolonged activation of microglia leads to the release of proinflammatory cytokines, initiating a proinflammatory cascade and subsequently contributing to neuronal damage and loss [53].”