Abstract
Monosialoganglioside GM1-bound amyloid β-peptides have been found in patients' brains exhibiting early pathological changes of Alzheimer's disease. Herein, we report the ability of non-micellar GM1 to modulate Aβ40 aggregation resulting in the formation of stable, short, rod-like, and cytotoxic Aβ40 protofibrils with the ability to potentiate both Aβ40 and Aβ42 aggregation.
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