Much of our recent work has also centered on characterizing the Aβ aggregation process and the molecular mechanisms of Aβ42-induced toxicity and neurodegeneration. The most significant outcome of our studies is the solid finding that the GxxxG motif, as part of the Aβ42 peptide, is a key region influencing the aggregation dynamics and the toxic properties of this disease-causing molecule. Thus, it is now clear that the GxxxG motif has a dual role in AD pathogenesis and thus represents a highly promising therapeutic target. As such, our ultimate goal is to assess whether and how this highly interesting interaction motif can be effectively and specifically targeted by small molecule therapeutics and to investigate these molecular events in depth.