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The accumulation of amyloid-β42 fibrils is a hallmark in patients with Alzheimer's disease. The small heat-chock protein αB-crystallin is known to co-exist with amyloid-β42 fibrils and prevent amyloid fibril formation. Amyloid-β42 fibrils arise and expand through different mechanisms of nucleation, however the targeted mechanism by αB-crystallin is yet to be determined. The aim of this project
