Description

Neuroinflammation as one of the pathogenic mechanisms concerning to the development of Alzheimer’s disease (AD) has aroused more attention since last decades. Amyloid beta (Aβ) peptide generation is supposed to be the initial event in AD progress, followed by neuronal impairment, neuroinflammation, and severe substantial neuronal dysfunction. Interleukin-1 receptor (IL-1R) as one of the most prevalent inflammatory mediated surface receptors, participates not only in peripheral inflammation but also in AD-related neuroinflammation. In microglia, IL-1R activation triggers the downstream signaling and the production of proinflammatory cytokines and chemokines. IL-1R signaling also participates in AD-related Aβ-induced inflammasome activation. Besides, IL-1R activation in neurons may increase APP non-amyloid pathway by modulation of APP α-secretase activity, which may prevent neurotoxic Aβ generation. Thus, the exact role of IL-1R signaling in AD development and neuronal functions is somehow tricky.

Chapter