RESUMEN
Alzheimer disease (AD) is a common neurodegenerative disease with pathological features of accumulated amyloid plaques, neurofibrillary tangles, and the significant inflammatory environment. These features modify the living microenvironment for nerve cells, causing the damage, dysfunction, and death. Progressive neuronal loss directly leads to cognitive decline in AD patients and is closely related to brain inflammation. Therefore, impairing inflammation via signaling pathways may facilitate either the prevention or delay of the degenerative process. Triptolide has been evidenced to possess potent anti-inflammatory effect. In this review, we elaborate on two signaling pathways (the NF-κB and Nrf2 signaling pathways) that are involved in the anti-inflammatory effect of triptolide.
