The Effect of Erythrosine B on Amyloid Beta aggregation in Alzheimer's Disease

Abstract

Alzheimer’s disease is known as the most common form of dementia with an increasing number of new cases each year. The promising therapeutic strategy is the reduction of neurotoxic Amyloid β (Aβ) fibrils in which aggregation causes AD. Among numerous small molecules investigated as Aβ aggregation modulator, erythrosine B (ER) has been shown a safety profile with low toxicity and high blood-brain barrier permeability1. Investigation into the mechanism of ER that inhibits the aggregation of Aβ was performed using MD simulation. Also by modifying ER into Eosin Y(EOY) and Fluorescein (FLN), where halogen was added and removed respectively, the mechanism of modified ER was also investigated. From the simulation, binding sites of three molecules on Aβ, the effect of the molecules of Aβ’s backbone, and the conformational change of Aβ binding residues with the molecules were studied. In conclusion, the results showed that halogen plays an important role in binding to Aβ and ER contains the most affective structure to inhibit the aggregation of Aβ.