ALZHEIMER's disease (AD), the most common cause of dementia is accompanied by progressive memory loss and other cognitive functions. The conditionis estimated to affect approximately 36 million people, worldwide. AD is characterized by the presence of extracellular amyloid b (Ab) deposits, intracellular neurofibrillary tanglesand senile plaques in the cortex, hippocampus, basal forebrain and amygdale. Neurofibrillary tangles formation is the result of intracellular fibrillar aggregation of the microtubule-associated protein tau that is hyperphosphorylated and oxidized. Senile plaques consist of insoluble fibrillar Ab. It is established that Ab is formed after sequential cleavage of amyloid precursor protein and secreted to the extracellular space. It also inhibits hippocampal long-term potentiation and disrupts the synaptic plasticity. In addition, Ab accumulation induces an elevation in levels of reactive oxygen species (ROS) in neurons, leading to apoptotic neuronal death in rats and mice. Studies showed that the accumulation of Ab in brain plays an important role in the pathophysiology of AD and a close correlation exits between Ab procedure and the neurodegeneration process of AD. There exists evidence suggesting that memory impairment in AD begins with changes in hippocampal synaptic functions and then gradually progresses to neurodegeneration and neuronal loss in these patients.