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. Author manuscript; available in PMC: 2008 Mar 31.
Published in final edited form as: Brain Res Brain Res Rev. 2005 Jan 8;49(1):1–21. doi: 10.1016/j.brainresrev.2004.11.005

Fig. 6.

Fig. 6

Signaling pathways that are involved in caspase activation during Alzheimer's disease. Caspase activation during Alzheimer's disease results in the cleavage of presenilin leading to an increase in the susceptibility of neurons to apoptosis with loss of β-catenin, poly(ADP-ribose)polymerase (PARP), and Bcl-2. Caspases can cleave amyloid precursor protein (APP) and the resulting C-terminal fragment C31 to produce hyperphosphorylation of tau protein (p-tau) as well as activation of glycogen synthase kinase-3β (GSK-3β). C31 and β-amyloid (Aβ) promotes the activation of caspases. Caspases also directly cleave tau protein to contribute to the formation of neurofibrillary tangles.