Protection of Si Nanowires against Aβ Toxicity by the Inhibition of Aβ Aggregation

TL;DR

This study shows that silicon nanowires can protect nerve cells from the toxic effects of amyloid beta, a key factor in Alzheimer's disease, by preventing its harmful aggregation.

Contribution

The novel contribution is demonstrating that Si nanowires inhibit Aβ aggregation and reduce neurotoxicity in a cellular model of Alzheimer's disease.

Findings

Si nanowires significantly reduced cell death in PC12 cells caused by Aβ1–42 oligomers.

Si nanowires inhibited Aβ aggregation by interfering with β-sheet structure formation.

Pre-incubation with Si nanowires provided neuroprotection against Aβ-induced toxicity.

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of amyloid beta (Aβ) plaques in the brain. Aβ1–42 is the main component of Aβ plaque, which is toxic to neuronal cells. Si nanowires (Si NWs) have the advantages of small particle size, high specific surface area, and good biocompatibility, and have potential application prospects in suppressing Aβ aggregation. In this study, we employed the vapor–liquid–solid (VLS) growth mechanism to grow Si NWs using Au nanoparticles as catalysts in a plasma-enhanced chemical vapor deposition (PECVD) system. Subsequently, these Si NWs were transferred to a phosphoric acid buffer solution (PBS). We found that Si NWs significantly reduced cell death in PC12 cells (rat adrenal pheochromocytoma cells) induced by Aβ1–42 oligomers via double staining with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and fluorescein diacetate/propyl iodide (FDA/PI). Most importantly, pre-incubated Si NWs largely prevented Aβ1–42 oligomer-induced PC12 cell death, suggesting that Si NWs exerts an anti-Aβ neuroprotective effect by inhibiting Aβ aggregation. The analysis of Fourier Transform Infrared (FTIR) results demonstrates that Si NWs reduce the toxicity of fibrils and oligomers by intervening in the formation of β-sheet structures, thereby protecting the viability of nerve cells. Our findings suggest that Si NWs may be a potential therapeutic agent for AD by protecting neuronal cells from the toxicity of Aβ1–42.

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