Platinum (II) Schiff Base Complexes and their Effects on the Inhibition of Amyloid β1–42 Aggregation.

For synthesizing metal–organic molecules with pro‐drug properties to prevent the accumulation of amyloid beta (Aβ1–42), which is a feature of neurodegenerative Alzheimer's disease, two new Schiff bases with imine/amine donors 2‐([3,3‐diphenylalidene]amino)‐N,N‐dimethylethane‐1‐amine and N,N‐dimethyl‐2‐([quinolin‐4‐ylmethylene]amino)ethane‐1‐amine, as well as their novel Pt (II) complexes (I and II), were synthesized and characterized via Fourier transform infrared spectroscopy, 1H‐ and 13C‐nuclear magnetic resonance (NMR) spectroscopy, mass spectrometry, and elemental analyses. The spectroscopic data has shown that the ligands are coordinated to the central atom in a chelating manner. Furthermore, the interaction between these complexes and Aβ1–42 was investigated using the electrochemical methods, square wave voltammetry and pencil graphite electrode, while monitoring the changes in the oxidation signal of the Try residue in Aβ1–42. The ability of the compounds to inhibit Aβ1–42 aggregation was investigated using the human neuroblastoma cell line (SH‐SY5Y). Complex II could actively inhibit the aggregation of Aβ1–42 at a molar ratio of 1.0/1.0, and its Aβ1–42 aggregation kinetics were fluorometrically determined using thioflavin T. These results were supported by scanning electron microscopy and transmission electron microscopy analyses. Moreover, the interaction of complex II with Aβ1–16 was investigated via 1H‐NMR spectroscopy. As a result, it was observed that complex II was effective in inhibiting the aggregation of Aβ1–42 at a molar ratio of 1.0/1.0. This result shows that studies can be conducted on the effects of Schiff base‐Pt complexes as potential pro‐drugs on Alzheimer's disease. [ABSTRACT FROM AUTHOR]