Alzheimer’s disease (AD) is one of the most devastating neurodegenerative diseases. Aggregation of amyloid-beta peptide (Aβ) into cytotoxic oligomers and fibrills is one of the major hallmarks in AD. These pathological depositions in the brain are thought to be one of the main causes for the observed progressive cognitive decline in AD patients.
Interfering with Aβ aggregation is an inevitable strategy in the development of novel therapeutic approaches. Reliable in vitro models are needed, which are capable of showing direct effects of compounds on Aβ oligomer formation and thus, a beneficial impact on cell viability.