Exploring the mechanism of beta-amyloid toxicity attenuation by multivalent sialic acid polymers through the use of mathematical models.

ABSTRACT: beta-Amyloid peptide (A beta), the primary protein component in senile plaques associated with Alzheimer's disease (AD), has been implicated in neurotoxicity associated with AD. Previous studies have shown that the A beta-neuronal membrane interaction plays a role in the mechanism of A beta toxicity. More specifically, it is thought that A beta interacts with ganglioside rich and sialic acid rich regions of cell surfaces. In light of such evidence, we have used a number of different sialic acid compounds of different valency or number of sialic acid moieties per molecule to attenuate A beta toxicity in a cell culture model. In this work, we proposed various mathematical models of A beta interaction with both the cell membrane and with the multivalent sialic acid compounds, designed to act

SUBMITTER: Cowan CB 

PROVIDER: S-EPMC2755187 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature