Role of the inflammatory response in Alzheimer’s disease
G. DERETZI , S.H. PELIDOU

Although the specific process that destroys neurons in Alzheimer’s disease (AD) remains obscure, immunohistological, molecular and epidimiological studies have greatly contributed to elucidating the role of the inflammatory response in the pathogenesis of neurogeneration in AD. Both the classical complement pathway and the alternate complement pathway are activated by amyloid β (Αβ) leading to the generation of a potent proinflammatory response. Inflammation is mediated through cytokines and other products of activated microglia. Αβ, along with interferon γ (IFN-γ), can trigger the production of reactive nitrogen intermediates and tumor necrosis factor α (TNF-α) in culture microglia, which leads to neuronal cell injury, as well as enhance microglial release of interleukin-1 (IL-1). This review summarizes the molecules, the complement-mediated inflammatory response, the neuroautoimmunity, the immune clearance mechanism and the role of microglial cells known at this point to be involved in the AD pathogenic process. This complexity of factors may offer points of therapeutic intervention for new types of antiinflammatory agents.

 Key words: Alzheimer’s disease, inflammation, cytokines.