There is growing evidence that an altered metabolism of the amyloid β (Aβ) precursor protein (APP) with progressive deposition of its Aβ fragment is a crucial event in the pathogenesis of AD. Increasing evidence suggests that inflammation and alteration of the cytokine-chemokine network contributes to the pathophysiology of AD. Activated microglia produce multiple pro-inflammatory cytokines, chemokines, and reactive oxygen species (ROS); additionally, Aβ itself can stimulate microglia, astrocytes, and oligodendrocytes to secrete pro-inflammatory cytokines, chemokines, and ROS, which can lead to neuronal damage. The concomitant release of pro-inflammatory cytokines, which influence neurodegenerative pathways, and anti-inflammatory cytokines may contribute to the chronicity of the disease. It is the balance of pro- inflammatory products and anti-inflammatory products that may be essential in the degenerative process. Influencing this balance may help in slowing the disease. Promising results for neurological disease treatment may be achieved by targeting cytokines and chemokines in the development of antagonists and synthesis inhibitors.