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Cause And Consequence Of Aβ – Lipid Interactions In Alzheimer Disease Pathogenesis, Vijayaraghavan Rangachari, Dexter N. Dean, Pratip Rana, Ashuwin Vaidya, Preetam Ghosh
Cause And Consequence Of Aβ – Lipid Interactions In Alzheimer Disease Pathogenesis, Vijayaraghavan Rangachari, Dexter N. Dean, Pratip Rana, Ashuwin Vaidya, Preetam Ghosh
Department of Mathematics Facuty Scholarship and Creative Works
Self-templating propagation of protein aggregate conformations is increasingly becoming a significant factor in many neurological diseases. In Alzheimer disease (AD), intrinsically disordered amyloid-β (Aβ) peptides undergo aggregation that is sensitive to environmental conditions. High-molecular weight aggregates of Aβ that form insoluble fibrils are deposited as senile plaques in AD brains. However, low-molecular weight aggregates called soluble oligomers are known to be the primary toxic agents responsible for neuronal dysfunction. The aggregation process is highly stochastic involving both homotypic (Aβ-Aβ) and heterotypic (Aβ with interacting partners) interactions. Two of the important members of interacting partners are membrane lipids and surfactants, to …
Determination Of Critical Nucleation Number For A Single Nucleation Amyloid-Β Aggregation Model, Preetam Ghosh, Ashuwin Vaidya, Amit Kumar, Vijayaraghavan Rangachari
Determination Of Critical Nucleation Number For A Single Nucleation Amyloid-Β Aggregation Model, Preetam Ghosh, Ashuwin Vaidya, Amit Kumar, Vijayaraghavan Rangachari
Department of Mathematics Facuty Scholarship and Creative Works
Aggregates of amyloid-β (Aβ) peptide are known to be the key pathological agents in Alzheimer disease (AD). Aβ aggregates to form large, insoluble fibrils that deposit as senile plaques in AD brains. The process of aggregation is nucleation-dependent in which the formation of a nucleus is the rate-limiting step, and controls the physiochemical fate of the aggregates formed. Therefore, understanding the properties of nucleus and pre-nucleation events will be significant in reducing the existing knowledge-gap in AD pathogenesis. In this report, we have determined the plausible range of critical nucleation number (n*, the number of monomers associated within the nucleus …