Figure 2: Proposed causes of apoptosis and the role of caspases and its inhibitors in Alzheimer’s Disease (AD): β Amyloid toxicity is the major cause of cell death in AD. β Amyloid peptides are generated from larger Amyloid Precursor Protein (APP) by the proteolytic actions of β and γ secretases. β amyloid causes cell death through inflammation, oxidative stress, as well as direct damage to the cell membrane. Death factors triggers mitochondria for the release of cytochrome c, this induces the activation of different apoptotic factors within the cell. Bcl2 family proteins includes a combination of pro-apoptotic (Bax, Bad, Bak) and anti-apoptotic (Bcl2,BclxL) proteins that regulate the permeability of mitochondrial membrane, regulating cytochrome c release. In the cytosol it combines with the Apoptotic Protease Activating Factor 1 (APAF1) and procaspase 9 to produce active caspase 9. Caspase 9 cleaves pro-caspase 3 to active caspase 3, that also induces other effector caspases. Caspases cleaves apoptotic substrates and causes DNA damage , resulting apoptosis. Lack of growth factor results in the activation of caspase 8, that can affect mitochondria as well as can form active caspase3.Caspase inhibitors stops the downstream caspase activation, as a result execution of apoptotic pathway get blocked and apoptosis cannot take place.