Alzheimer's disease is one of the most widespread neurodegenerative disorder. The etiology of this disease is not completely elucidated. Amyloid plaques (extracellular aggregates of amyloid β peptides – Aβ) and neurofibrillary tangles (intracellular deposits of hyperphosphorylated tau protein) are histopa- thological hallmarks of the Alzheimer disease. These morphological changes are present mostly in brain regions involved in cognition, emotion, learning and memory. The critical events in the pathogenesis of Alzheimer's disease are caused by amyloid β peptides. The mechanism of the neurotoxicity of Aβ has not yet been fully defined. Aβ peptides have been reported to mediate dysfunction of mitochondria, produc- tion of reactive oxidative species and disruption of cell membrane permeability. Proteolytic processing of the amyloid precursor protein (APP) by β- and γ-secretase is the initial step in the production of the amyloid β peptide, it occurs throughout the whole life. Attenuated mechanisms of the Aβ maintenance on non-toxic level in the brain, is the main cause of Alzheimer's disease. The genetics and environmental risk factors associated with this disorder have been characterized. Moreover, Aβ permanently presented in brain of people suffering from Alzheimer's disease stimulates chronic inflammatory reaction, which might contribute to death of neurons. However, many evidences indicate that mediators of inflammatory reaction have beneficial effects on neuron survival in Alzheimer's disease. The contribution of inflamma- tory processes to Alzheimer's disease remains to be elucidated. Recently, the rapid progress towards understanding of Alzheimer's disease molecular mechanisms have been made. On the basis of current knowledge many new therapeutics strategies are developed.