Role of genes linked to sporadic Alzheimer's disease risk in the production of β-amyloid peptides.

Bali J, Gheinani AH, Zurbriggen S, Rajendran L.
Journal   Proc Natl Acad Sci U S A.
Species  
Analytes Measured   Abeta 38 , Abeta 40 , Abeta 42 , APP
Matrix Tested   Cell culture supernatants
Year   2012
Volume  
Page Numbers  
Application   Alzheimers
Abstract
Alzheimer's disease (AD) is characterized by the presence of toxic protein aggregates or plaques composed of the amyloid β (Aβ) peptide. Various lengths of Aβ peptide are generated by proteolytic cleavages of the amyloid precursor protein (APP). Mutations in many familial AD-associated genes affect the production of the longer Aβ42 variant that preferentially accumulates in plaques. In the case of sporadic or late-onset AD, which accounts for greater than 95% of cases, several genes are implicated in increasing the risk, but whether they also cause the disease by altering amyloid levels is currently unknown. Through loss of function studies in a model cell line, here RNAi-mediated silencing of several late onset AD genes affected Aβ levels is shown. However, unlike the genes underlying familial AD, late onset AD-susceptibility genes do not specifically alter the Aβ42/40 ratios and suggest that these genes probably contribute to AD through distinct mechanisms.

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