Neuroinflammation-related signaling pathways

Neuroinflammation-related signaling pathways encompass a diverse set of molecular cascades, including the NF-kappaB, JAK/STAT, and NLRP3 inflammasome pathways, which coordinate the immune response within the central nervous system (Liu et al., 2017, Frontiers in Molecular Neuroscience). These pathways are primarily mediated by microglia and astrocytes, which transition to a pro-inflammatory state in response to stimuli like amyloid-beta plaques or myelin debris (Heneka et al., 2013, Nature). While acute activation is protective, chronic neuroinflammation is a pathological hallmark of neurodegenerative disorders such as Alzheimer's and Parkinson's disease, leading to progressive neuronal damage (Qin et al., 2016, Journal of Neuroinflammation). Therapeutic strategies aim to inhibit these pathways using small molecules or biologics to reduce the secretion of neurotoxic cytokines like TNF-alpha and IL-1beta. However, because these pathways are also involved in synaptic pruning and tissue homeostasis, their modulation carries risks of impairing normal brain function or increasing susceptibility to infections (Zetterberg & Bendel, 2021, Nature Reviews Neurology).

Other names

Neuroinflammatory pathwaysCNS inflammatory signalingGlial activation cascades

Inhibition of pro-inflammatory cytokine production, modulation of glial activation, and blockade of intracellular signaling cascades such as NF-kappaB and JAK/STAT.