A gold nanoparticle-mediated rapid in vitro assay of anti-aggregation reagents for amyloid β and its validation

Kim, Hye Young; Lee, Donghee; Ryu, Kwon‐Yul; Choi, Inhee

doi:10.1039/c7cc00358g

Cited by 13 publications

(10 citation statements)

References 48 publications

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“…Aβ-GNP aggregation, 26 previous studies have suggested that the electrostatic interaction between Aβ and GNPs plays a significant role in Aβ-GNP aggregation through rapid aggregate formation under acidic pH conditions (pH 2− 3). 21,25 However, our observation suggested that acidic pH can disrupt colloidal states of GNPs and produce the SPR red shifting that is identical to the one generated by Aβ-GNP aggregation. Previous studies also showed that colloidal dispersion of GNPs is influenced by pH and ionic strength.…”

Section: Although Various Intermolecular Interactions Can Influencementioning

confidence: 71%

“…For Aβ aggregation, the 9:1 ratio of Aβ 40 and Aβ 42 was used as suggested in a previous study . Briefly, 10 μM Aβ 40 and 10 μM Aβ 42 solution was prepared fresh in 1× PBS from the stock solution (1 mg/mL) before use.…”

Section: Methodsmentioning

confidence: 99%

“…For Aβ aggregation, the 9:1 ratio of Aβ 40 and Aβ 42 was used as suggested in a previous study. 21 Briefly, 10 μM Aβ 40 and 10 μM Aβ 42 solution was prepared fresh in 1× PBS from the stock solution (1 mg/mL) before use. The diluted 10 μM Aβ peptides were briefly spun down and mixed to a 9:1 ratio (v/v) to make the working solution for Aβ aggregation.…”

Section: ■ Introductionmentioning

confidence: 99%

“…Nanoparticles have been used in a wide range of applications. − Recent studies have shown that plasmonic gold nanoparticles (GNPs) have great potential as the inhibitor screening tool for proteins with aggregation propensity , by accelerating the protein aggregation as a catalyst while providing real-time information on the aggregation states by surface plasmon resonance (SPR) shifting and color changes without the need for additional probes. − …”

Section: Introductionmentioning

confidence: 99%

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Surface Plasmon Resonance Assay for Identification of Small Molecules Capable of Inhibiting Aβ Aggregation

Lee

Lim

2021

ACS Appl. Mater. Interfaces

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Toxic aggregates of amyloid-beta (Aβ) have importance in the pathology of Alzheimer’s disease, and inhibition of aggregate formation is considered to be a promising strategy for drug development. Here, we report a simple and rapid surface plasmon resonance (SPR) assay method that can identify potential Aβ aggregation inhibitors. Our assay is based on the SPR shifting of the Aβ-gold nanoparticle (Aβ-GNP) aggregates by size under the influence of an Aβ aggregation inhibitor. This user-friendly assay features a short assay time with a low reagent consumption that can be easily adapted as a high-throughput screen. We demonstrated that an effective Aβ aggregation inhibitor induces the blue-shifted SPR peaks of the Aβ-GNP aggregates by hindering the formation of long fibrillar aggregates. Moreover, the blue shifting was correlated to the efficacy and concentrations of an Aβ aggregation inhibitor. Overall, our findings suggest that our simple SPR assay can be a powerful tool to screen small molecules targeting Aβ aggregation.

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Section: Although Various Intermolecular Interactions Can Influencementioning

confidence: 71%

Section: Methodsmentioning

confidence: 99%

Section: ■ Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Surface Plasmon Resonance Assay for Identification of Small Molecules Capable of Inhibiting Aβ Aggregation

Lee

Lim

2021

ACS Appl. Mater. Interfaces

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“…et al(Kim et al 2017) suggested that AuNPs could act as an effective gene regulator and decrease the aggregation of Aβ. In addition, AuNPs have a protective effect on Aβ1-42-induced apoptosis, and the process is related to NF-KB-induced neuroin ammation(Ali et al 2016).…”

mentioning

confidence: 99%

Protective mechanism of gold nanoparticles on human neural stem cells injured by β-amyloid protein

Wang

Shen

Song

et al. 2022

Preprint

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BACKGROUND AND PURPOSE Alzheimer’s disease (AD) is a neurodegenerative disorder with progressive memory loss in dementia. Gold nanoparticles (AuNPs) were reported beneficial for human neural stem cells (hNSCs) treated with Amyloid-beta (Aβ), but the neuroprotective mechanisms still are unknown. METHODS Cell Counting Kit-8 (CCK-8) was performed to detect hNSCs viability. The content of interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) was analyzed by enzyme-linked immunosorbent (ELISA) assay. Immunocytochemistry was carried out to determinate Tuj-1 and glial fibrillary acidic protein (GFAP). The reactive oxygen species (ROS) and JC-1 assay kits were performed to detect ROS generation and mitochondrial membrane potential. Quantitative PCR (qPCR) and Western blot assessments were also used to detect related gene expression intracellularly or in the supernatant. RESULTS The pro-inflammation IL-6 and TNF-α were significantly decreased in the AuNPs co-treatment group. AuNPs could ameliorate neural stem cell differentiation inhibition due to Aβ accumulation. AuNPs co-treatment repressed the high expression of total tau (T-tau), phosphorylated tau (P-tau), and Aβ protein caused by the Aβ treatment. The apoptosis rate of hNSCs induced by Aβ was inhibited by AuNPs co-treatment and the expression of proteins associated with apoptosis was also reduced in AuNPs co-treatment group. Aβ-induced decreased mitochondrial membrane potential and mitochondria in the hNSCs were damaged, while AuNPs co-treatment showed the protective effect on mitochondrial membrane potential. Co-treatment with AuNPs significantly increased dynamin-related protein 1 (DRP1), nuclear respiratory factor 1 (NRF1), and mitochondrial transcription factor A (TFAM) mRNA level. AuNPs may improve mitochondrial function impairment due to Aβ by elevating mitochondrial membrane potential, upregulating regulators of mitochondrial biogenesis, and inhibiting ROS production. hNSCs transfected with miR-21-5p inhibitor reversed AuNPs mediated cytoprotection induced by Aβ. miR-21-5p was involved in AuNPs protecting against Aβ-induced cell toxicity by reduced mitochondrial function. CONCLUSION AuNPs can protect hNSCs from Aβ injury by up-regulating miR-21-5p and protecting mitochondrial function.

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Gold Nanoparticles in Diagnosis and Treatment of Alzheimer’s Disease

Sivanesan

Rajeshkumar

2019

Nanobiotechnology in Neurodegenerative Diseases

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A gold nanoparticle-mediated rapid in vitro assay of anti-aggregation reagents for amyloid β and its validation

Cited by 13 publications

References 48 publications

Surface Plasmon Resonance Assay for Identification of Small Molecules Capable of Inhibiting Aβ Aggregation

Surface Plasmon Resonance Assay for Identification of Small Molecules Capable of Inhibiting Aβ Aggregation

Protective mechanism of gold nanoparticles on human neural stem cells injured by β-amyloid protein

Gold Nanoparticles in Diagnosis and Treatment of Alzheimer’s Disease

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