Astrocyte-derived CCL7 promotes microglia-mediated inflammation following traumatic brain injury.

Microglia are immune cells of the central nervous system that mediate neuroinflammation. It is widely known that microglia-mediated inflammation in the brain contribute to the widespread tissue damage and neurological deficits in traumatic brain injury (TBI). However, the mechanisms responsible for this inflammatory response remain elusive.

Mitochondrial dysfunction and apoptosis are attenuated through activation of AMPK/GSK-3β/PP2A pathway in Parkinson's disease.

Parkinson's disease (PD) is a common neurological disorder worldwide, characterized by loss of dopaminergic neurons and decrease of dopamine content. Mitochondria plays an important role in the development of PD. Adenosine 5'-monophosphate-activated protein kinase (AMPK), glycogen synthase kinase 3 (GSK-3β) and protein phosphatase 2A (PP2A) are all key proteins that regulate mitochondrial metabolism and apoptosis, and they are involved in a variety of neurodegenerative diseases.

The role of TLR2/JNK/NF-κB pathway in amyloid β peptide-induced inflammatory response in mouse NG108-15 neural cells.

The TLR2-mediated neuroinflammatory activation has been involved in the pathogenesis of Alzheimer's disease (AD) associated with amyloid β(Aβ) deposition. In neuronal damage, JNK and NF-κB pathways contribute to TLR2-dependent secretion of proinflammatory cytokines. However, the role of TLR2/JNK/NF-κB pathway on Aβ-induced inflammatory response in nerve cell damage remains unclear.