Abnormal amyloid beta (Aβ) aggregation in the form of plaques and its deposition across the human nerve cells are a major hallmark of Alzheimer’s disease. Aβ aggregation dynamics and, more importantly, various drugs’ effects, either to inhibit the fibril aggregation or to degrade the mature fibrils, have been an area of active research. Large molecule (peptide-based) inhibitors, such as decapeptide (RYYAAFFARR) and pentapeptide (LPFFD), show inhibition/degradation effects on amyloid beta fibrils. Herein, a mathematical model has been proposed. The model simulates Aβ aggregation and inhibitory/degradative action of peptide inhibitors on Aβ fibrillation. Model parameters are tuned by curve fitting the experimental data. The tuned model is used to predict experimental data at different initial dose/fibril concentrations. Model predicted results are observed to be in good agreement with the reported experimental data, demonstrating model’s applicability at the molecular level. Sensitivity analyses of the model parameters on the fibril concentration further establish the robustness of the proposed model.
