Amyloid β, Aβ(1–42), is a component of senile plaques present in the brain of Alzheimer’s disease patients and one of the main suspects responsible for pathological consequences of the disease. Herein, we directly visualize the Aβ activity toward a brain-like model membrane and demonstrate that this activity strongly depends on the Aβ oligomer size. PeakForce quantitative nanomechanical mapping mode of atomic force microscopy imaging revealed that the interaction of large-size (LS) Aβ oligomers, corresponding to high-molecular-weight Aβ oligomers, with the brain total lipid extract (BTLE) membrane resulted in accelerated Aβ fibrillogenesis on the membrane surface. Importantly, the fibrillogenesis did not affect integrity of the membrane. In contrast, small-size (SS) Aβ oligomers, corresponding to low-molecular-weight Aβ oligomers, created pores and then disintegrated the BTLE membrane. Both forms of the Aβ oligomers changed nanomechanical properties of the membrane by decreasing its Young’s modulus by ∼45%. Our results demonstrated that both forms of Aβ oligomers induce the neurotoxic effect on the brain cells but their action toward the membrane differs significantly.
A new redox conducting polymer, viz. poly[meso-N,N′-bis(salicylidene)-2,3-butanediaminonickel(II)], poly[meso-Ni(II)-SaldMe], belonging to the Schiff base polymer family, was electrochemically synthesized. The charge transfer and polymerization mechanism were unraveled by simultaneous cyclic voltammetry (CV) and in situ UV–vis, FTIR-ATR, and ex situ low-temperature ESR spectroscopy. With the latter, a short-living paramagnetic transient form of electro-oxidized poly[meso-Ni(II)-SaldMe] was detected. This form was identified as the bisphenolic radical cation. In situ UV–vis and FTIR-ATR spectroelectrochemistry measurements revealed that the charge transfer of the polymer involved bisphenolic radical cation formation at the potential lower than 0.80 V vs Ag/Ag+ and then dication formation at the potential exceeding 0.80 V. The proposed mechanism of electropolymerization of meso-N,N′-bis(salicylidene)-2,3-butanediaminonickel(II), meso-Ni(II)-SaldMe, involves two steps. First, electro-oxidation of the monomer results in bisphenolic radical cation generation, and then mutual binding of these radicals at the para positions of aromatic rings is activated by electron-donating phenol moieties. In this electropolymerization, the Ni(II) metal center played the role of a template providing planarity to the monomer molecule. Structures responsible for the charge transfer in the polymer and formed during electropolymerization were modeled with quantum chemistry calculations using the DFT method at the PBE level. The resulting polymer film was highly conducting and stable with respect to potential multicycling under cyclic voltammetry conditions, from 0 to 1.3 V vs Ag/Ag+. Under these conditions, it changes color from yellow through orange to russet for its neutral, bisphenolic radical cation, and bisphenolic dication form, respectively. High electrochemical stability and a wide potential range of electroactivity (0.40–1.30 V vs Ag/Ag+) of the polymer are very promising for its application as a new electrochromic electrode material for supercapacitors. That is, an anode composed of poly[meso-Ni(II)-SaldMe] can serve as an internal charging–discharging indicator in these supercapacitors.
The “gate effect” mechanism for conductive molecularly imprinted polymer (MIP) film coated electrodes was investigated in detail. It was demonstrated that the decrease of the DPV signal for the Fe(CN)6 4–/Fe(CN)6 3– redox probe with the increase of the p-synephrine target analyte concentration in solution at the polythiophene MIP-film coated electrode did not originate from swelling or shrinking of the MIP film, as it was previously postulated, but from changes in the electrochemical process kinetics. The MIP-film coated electrode was examined with cyclic voltammetry (CV), differential pulse voltammetry (DPV), electrochemical impedance spectroscopy (EIS), and surface plasmon resonance (SPR). The MIP-film thickness in the absence and in the presence of the p-synephrine analyte was examined with in situ AFM imaging. Moreover, it was demonstrated that doping of the MIP film was not affected by p-synephrine binding in MIP-film molecular cavities. It was concluded that the “gate effect” was most likely caused by changes in radical cation (polaron) mobility in the film.
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