Abstract
In the process of toxic accumulation of Amyloid-beta (Aβ) peptides in plaques, problems may arise in the exchange of nutrients across the blood–brain barrier (BBB) level and impaired brain clearance. These plaques are associated with the progression of Alzheimer’s disease (AD). A four-compartmental model to describe the alteration of Aβ transport across BBB level and its accumulation in the brain is presented here. Furthermore, potential target mechanisms of therapy, to counteract the disease progression, are investigated using an’in silico’ approach. A sensitivity analysis is presented to show the most important parameters on which to act in order to potentially bring pathological conditions back to non-pathological ones.
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