Philip Dopp, BSc

Alzheimer's Disease (AD) is a neurological disorder that is characterized by a slowly degenerative process affecting cognitive function. At a histopathological level, AD patients are characterized by the deposition of senile plaques within the brain, as well as within the walls of cerebral blood vessels.^1-5 It is believed that through an unknown mechanism, these senile plaques exert a toxic effect on surrounding neurons, resulting in the neuronal degeneration found in AD patients.^1,5

The primary constituent of these senile plaques is amyloid b peptide (Ab). Two proteases, b-secretase and g-secretase cleave this peptide from a larger precursor protein, b-amyloid precursor protein (APP).^1,5-6 Essentially, b-secretase cleaves APP to produce an APPsb soluble fragment and C99, a membrane bound fragment, whereas a-secretase can prohibit Ab formation by cleaving APP within the Ab sequence to produce APPsa and C83.⁶ Ultimately, g-secretase acts on C99 to produce Ab, or on C83 to produce a nonpathogenic p3 peptide.