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 to stimulate the inflammatory responsecorrelative with expression ofiNOS, the activation of the NFκB signal pathway and the expression ofiNOS,which results in significant peroxynitrite damage to neurons and the neurodegeneration in Alzheimer's disease (AD). Activation of CD36 signaling in microgila by Aβ fibrils initiates the association of the Src-family kinase Lyn with CD36. Together with another Src kinase, Fyn, Lyn activates a MAPK signaling response and results in the activation of inflammatory programs such as the production of MCP-1 and ROS.In parallel, Syk-family kinase activity specifically regulates increased cytokine production in response to Aβstimulation. After the stimulation, NFκB works independent of Src and Syk activation. Aβ-stimulated microglial secretes TNF-α and O2-, resulting in iNOS overexpression and excessive peroxynitrite and neuronal apoptosis.