Beta Amyloid peptide (A?), specifically A? (1-42) is toxic to neurons and is hence strongly associated with loss of brain function through the course of Alzheimer’s disease. This deposition induces neuronal death and apoptosis. Extensive studies in recent years have focused on A?-mediated microglia activation with regard to secretion of pro inflammatory cytokines such as TNF-?. TNF-? induces two distinct pathways: one of them is apoptosis and the other one is NF-?B activation and eventually cell survival and proliferation.One of the questions that came to us was whether there is any relationship between these two path ways and blocking one pathway results in boosting the other one. To probe this issue, we blocked apoptosis and measure NF-?B activation. Another question arose as the role of apoptosis in neuroinflammation. Whether apoptosis is a protective or destructive mechanism? To achieve this goal, we inhibited apoptosis and evaluated some intracellular changes such as: c-Myc as a proto-oncogene, Hsp70 as a hallmark of cancer that is up regulated by stress and toxins and p53 as a tumor suppressor protein.