Neuroinflammation in Alzheimer’s Disease: the Regulatory Effects of TNF-α
CHEN Zirun1, ZHU Junzhe1, QIAN Jingkang1, ZHANG Lihan1, PAN Xuyi1, MIAO Xuemeng2, HUANG Zhihui1, 3*, XU Haiyun1*
AD (Alzheimer’s disease) is a neurodegenerative disease, its pathogenesis involves amyloidβ deposition leading to senile plaques in the brain, overphosphorylated Tau protein accumulates in nerve cells to form neurofibrillary tangles, axonal degeneration, etc. There is growing evidence, however, showing the pathogenesis of AD is not limited to neurons, but is also closely related to glial cells in brain tissue. Indeed, microglia and astrocytes play multiple roles in the neuroinflammatory process thus influencing the onset,development, and outcome of AD. Microglia and astrocytes secrete many cytokines and chemokines in the process of neuroinflammation, among which TNF-a specifically binds to the cell surface receptors TNFR1 and TNF-R2, followed by the activation of NF- кВ, JNK (c-Jun) and other signaling pathways promoting the expression of more inflammatory cytokines, what’s more, impacting multiple pathological processes such as inflammation induction, apoptosis, APР and Tau protein production. This paper aims to review the role and mechanism of glial cells and TNF-a in regulating neuroinflammation in AD.
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