p38 MAPK Is a Major Regulator of Amyloid Beta-Induced IL-6 Expression in Human Microglia

• Published in: Molecular neurobiology Vol. 59; no. 9; pp. 5284 - 5298
• Main Authors: Lin, Houmin, Dixon, Steven Grant, Hu, Wei, Hamlett, Eric D., Jin, Junfei, Ergul, Adviye, Wang, Gavin Y.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.09.2022; Springer Nature B.V
• Subjects: Alzheimer Disease - metabolism; Alzheimer's disease; Amyloid beta-Peptides - metabolism; Biomedical and Life Sciences; Biomedicine; Cell Biology; Humans; Immunoreactivity; Inflammation; Interleukin 6; Interleukin-6 - metabolism; Kinases; Localization; MAP kinase; Microglia; Microglia - metabolism; Microglial cells; Neurobiology; Neurodegenerative diseases; Neurology; Neurosciences; p38 Mitogen-Activated Protein Kinases - metabolism; Patients; Plaque, Amyloid - metabolism; Protein kinase; Senile plaques; Tumor necrosis factor-α; Neuroinflammation; Amyloid beta; Alzheimer’s disease; p38 MAPK; Microglia; Interleukin-6

The accumulation of amyloid beta (Aβ) plaques in the brain is a hallmark of Alzheimer’s disease (AD) pathology. Microglial activation-mediated neuroinflammation has been implicated in the pathogenesis of AD and the expression levels of interleukin-6 (IL-6) were increased in the brains of AD patients...