Alzheimer's disease (AD) is an irreversible, progressive and degenerative disorder that destroys the higher structures of the brain. Prominent neuropathologic features of AD are senile plaques, neurofibrillary tangles, synaptic and neuronal loss. There is mounting evidence that chronic inflammatory processes play a fundamental role in the progression of neuropathological changes of AD. It has been shown, that there is a reciprocal relationship between the local inflammation and senile plaques (SPs) and neurofibrillary tangles (NFTs). The major players involved in the inflammatory process in AD are thought to be the microglia and the astrocytes. The process of the activation of glia is characteristized by upregulation or newly expression of a variety of molecules involved in inflammatory response including cytokines, various components of the complement cascade, acute phase reactants, proteases and protease inhibitors, and neurotoxic products. The importance of inflammation in the pathogenesis of AD was indirectly confirmed by epidemiological investigations that revealed a decreased incidence of AD in subjects using anti-inflammatory drugs, especially the non-steroidal anti-inflammatory drugs (NSAIDs). However clinical trials designed to inhibit inflammation have failed in the treatment of AD patients suggesting that anti-inflammatory agents have more protective than therapeutic effect. Despite the ongoing research the extent to which neuroinflammation contributes to disease pathogenesis is still not fully understood. Moreover it is also not clear whether the inflammation in AD brains represent a protective reaction to neurodegeneration or it is rather a destructive process that contributes to further loss of brain function. (Ref. 117).