Magnetic field-boosted electrocatalytic process for the dissociation of Alzheimer's β-amyloid aggregates

Magnetic field-boosted electrochemistry has recently emerged as an effective strategy to enhancing the catalytic capability in industrially profitable purposes. However, its utilization to enhance the quality of life of individuals has not been thoroughly investigated yet. Here, we have unveiled a static magnetic field-boosted electrocatalytic process for the dissociation of self-assembled beta-amyloid (A beta) aggregates, the major pathological hallmark of Alzheimer's disease (AD). Cobalt-doped titanium oxide (Co-TiO2) electrode exhibits the repetitive boosting and recovery of electrical current density in response to an applied static magnetic field due to ferromagnetic cobalt dopants. According to our microscopic and spectroscopic analyses results, Co-TiO2 electrode successfully triggers the dissociation process of A beta aggregate structure only with applied voltage. Besides, the dissociation efficacy of Co-TiO2 electrode against A beta aggregates is boosted when a static magnetic field is applied in addition to the voltage. Our in vitro evaluation results demonstrate that Co-TiO2 electrode has biocompatibility and mitigating effect against A beta-associated neurotoxicity. Also, our ex vivo evaluation results confirm that Co-TiO2 electrode can clear micrometer-sized and accumulated A beta aggregates from AD mouse brain tissue. This work discovers a therapeutic potential of static magnetic field-boosted bioelectrocatalysis for future AD treatment.

Automated summary

This study reveals the effect of magnetic field-boosted bioelectrocatalysis on the dissociation of Aβ aggregates, the pathological hallmark of Alzheimer's disease. The Co-TiO2 electrode successfully triggers the dissociation process of Aβ aggregates with applied voltage, and the dissociation efficacy is enhanced when a static magnetic field is applied. In vitro and ex vivo evaluation results confirm the mitigating effect of the Co-TiO2 electrode on Aβ-associated neurotoxicity, as well as its ability to clear Aβ aggregates from AD mouse brain tissue.