Alzheimer’s disease (AD) is the most common form of dementia among the elderly population. AD, which is characterized as a disease of cognitive deficits, is mainly associated with an increase of amyloidβ-peptide (Aβ) in the brain. A growing body of recent studies suggests that protein kinase C (PKC) promotes the production of the secretory form of amyloid precursor protein (sAPPα) via the activation ofα-secretase activity, which reduces the accumulation of pathogenic Aβlevels in the brain. Moreover, activation of PKCαand mitogen-activated protein kinase (MAPK) is known to increase sAPPα. A novel type of PKC, PKCε, activates the Aβdegrading activity of endothelin converting enzyme type 1 (ECE-1), which might be mediatedviathe MAPK pathway as well. Furthermore, dysregulation of PKC-MAPK signaling is known to increase Aβlevels in the brain, which results in AD phenotypes. Here, we discuss roles of PKC in Aβproduction and clearance and its implication in AD.
Activation of protein kinase C modulates BACE1-mediated β-secretase activity
