Fig. 2.

Alzheimer's disease.

Above is a figure illustrating mitochondrial affecting pathways in Alzheimer's disease associated with Aβ, tau, Drp1, SIRT proteins, and Nrf2. Aβ and AβAD work synergistically to increase mitochondrial ROS, inhibit the CAC, and inhibit complexes 3 and 4 of the ETC. Aβ inhibitors inhibit Aβ and inhibit this synergistic activity. NADH and DH inhibit Aβ and AβAD synergy as well. Tau protein increases mitochondrial ROS and inhibits complexes 1, 4, and 5 of the ETC. Tau also increases the activity of VDAC, leading to the loss of the mitochondrial membrane potential. Tau inhibitors inhibit the tau protein. Drp1 works synergistically with GTPase to increase mitochondrial fission. Drp1 and tau inhibitors inhibit this activity. SIRT4 inhibits CAC. SIRT5 inhibits PDH while SIRT3 activates PDH. ROS activates the Keap1, Nrf2 complex. Nrf2 dissociates and enters the nucleus, where it increases transcription for antioxidants to inhibit ROS. SOD, CAT, mGSH, and empagliflozin also inhibit ROS.