ABSTRACT
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a selective neuronal loss and the presence of abnormal extracellular accumulation of β-amyloid peptide (AβP) in the sensitive structures of the brain. AβP derives from a type I integral membrane amyloid precursor protein (APP), by two consecutive proteolytic cleavages operated by β-and γ-secretase (Selkoe 2001). After the β-secretase enzyme cleaves the APP extracellular domain, γ-secretase cleaves the remaining segment to release the AβP.
