However, different diseases affect distinct regions of the brain, resulting in divergent clinical manifestations. Neuronal loss is progressive cell death or apoptosis, there are at least three hypotheses to explain this phenomenon. The widely accepted hypothesis is increased toxic activity that protein misfolding and aggregation results in neurotoxicity. Direct evidence is that aggregation of misfolded proteins in vitro can cause neuronal apoptosis (Claudio, 2003). This theory on the neurotoxicity of the beta-amyloid protein has four types of interpretation. First, it is possible that the extracellular aggregated protein could interact with specific receptors, activating a signaling pathway that can lead to apoptosis. The second is the intracellular aggregated protein that causes the recruitment of cellular factors and thus damages cells. The third is amyloid beta protein and prion protein which form neurotoxicity due to the formation of ion channels causing membrane disruption and depolarization which results in the change of ion homeostasis and regulation of cell signaling, leading to cell death. The fourth is the aggregation of proteins caused by oxidative stress, through the generation of free radicals, causing the oxidation of proteins and lipids and increasing the intracellular concentration of calcium ions and therefore the