Overview:

Amyloid peptides, derived from amyloid precursor protein (APP), are thought to play a role in the development of the senile plaques associated with Alzheimer’s Disease.The amyloid hypothesis presupposes that flaws in the processing of APP result in abnormally high levels of the longer, “stickier” forms of beta amyloid, known as Abeta42 and Abeta43, leading to aggregation of amyloid in the neuronal cell death and ultimately neuronal death.Mutations in the structure of Abeta40 and related peptides as well as in some of the enzymes involved in the processing of APP have been shown to alter the processing of APP. The sporadic (i.e., non-genetic) form of the disease, however, is far more common, caused by aging in concert with a number of both genetic and environmental risk factors.

References:

1. Esler WP, et al: Stereochemical specificity of Alzheimer's disease beta-peptide assembly. Biopolymers. 1999 May;49(6):505-14.2. Roher AE, et al: beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease.Proc Natl Acad Sci U S A. 1993 Nov 15;90 (22):10836-40.