Abstract
：Amyloid β-peptide (Aβ) stimulating inducible nitric oxide synthase (iNOS)induces neuron death or apoptosis through the transcription factor NFκB (nuclear factor κB) signal pathway mechanism. Aβ functiones together with microglia and astrocyte tostimulate the inflammatory responsecorrelative with expression ofiNOS, the activation ofthe NFκB signalpathway and the expression ofiNOS,which results in significant peroxynitrite damage toneurons and the neurodegeneration in Alzheimer's disease (AD). Activation of CD36signaling in microgila by Aβ fibrils initiates the association of the Src-family kinase Lyn withCD36. Together with another Src kinase, Fyn, Lyn activates a MAPK signaling response andresults in the activation of inflammatory programs such as the production of MCP-1 andROS.In parallel, Syk-family kinase activity specifically regulates increased cytokineproduction in response to Aβstimulation. After the stimulation, NFκB works independent of Src and Syk activation. Aβ-stimulated microglial secretesTNF-α and O2-,resulting in iNOS overexpression and excessive peroxynitrite and neuronal apoptosis. Key words: Nitric-oxide synthase; NF
Published Version
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