Background

Alzheimer’s Disease is a neurodegenerative disease, a hallmark of which is the accumulation of amyloid-beta (Alpha, Beta) oligomers in the synapses of mitochondria. This accumulation of amyloid-beta (Alpha, Beta) oligomers impairs various mitochondrial functions such as cellular respiration, energy metabolism and calcium homeostasis. In addition, amyloid-beta accumulation affects the permeability of the Mitochondrial Permeability Transition pore (mPTP). Amyloid-beta -induced dysfunction of the mitochondria is believed to be one of the mechanisms through which Amyloid-beta accumulation causes toxicity in Alzheimer’s Disease. Cyclophilin D (CypD) is an isomerase associated with the mitochondrial membrane that is overexpressed in Alzheimer’s Disease. CypD is known to play a central role in opening the mPTP, which can cause cell death. Together this suggests that CypD