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Creative Biolabs

Amyloid-beta Induced Toxicity Assay Service

Our Amyloid-beta (Aβ) induced toxicity assay service is applicable to a variety of research areas, including drug development, gene expression studies, and evaluation of new therapeutics. For more information on the products and services provided, project-specific consultations, and pricing, please submit an inquiry here.

Introduction

Distributed under Open Access license CC BY-SA 4.0, from Wiki, without modification.

Aβ is a key target in Alzheimer's disease (AD) research, and its abnormal accumulation is closely linked to neurodegenerative diseases. Aβ has toxic effects both inside and outside cells, and can induce pathological changes such as neuronal apoptosis, oxidative stress, and mitochondrial dysfunction. The interaction between Aβ and tau protein is also thought to be a key factor in the induction of neurotoxicity.

Available Assays at Creative Biolabs

Our amyloid-β-induced toxicity assay service can help customers evaluate the effects of different concentrations and forms of Aβ on neuronal cells. For example, cell viability and cytotoxicity can be accurately determined using methods such as the MTT assay and the LDH assay. In addition, interfacial studies can be performed using advanced nanomaterial technology to explore the assembly and toxicity mechanisms of Aβ under different conditions. We offer a variety of conventional methods for the evaluation of Aβ neurotoxicity, including but not limited to:

  • MTT assay
  • Propidium Iodide (PI) Assay
  • Lactate dehydrogenase (LDH) assay
  • Trypan Blue Assay
  • TUNEL assay

Advantages

  • Comprehensiveness: Our services cover toxicity assessments in various forms, from Aβ monomers and oligomers to fibrils, and can simulate neurotoxicity in various pathological states.
  • Accuracy: High-throughput screening technology and advanced biosensors are used to ensure the reliability and reproducibility of experimental results.
  • Innovation: Combining the latest nanotechnology and molecular probes, we provide customers with cutting-edge experimental tools and methods to help unravel the complex toxicity mechanism of Aβ.

Case Study: Measuring Aβ42 Oligomer (AβO) Toxicity to Hippocampal Neurons

To investigate the toxicity of different Aβ42s, 10 μm Aβ42 oligomers (AβO), 10 μm mature (AβF), and sonicated 10 μm Aβ42 fibrils (AβSon) were incubated with primary hippocampal neurons for 72 h. The results showed that after 72 h, the uptake efficiency of AβSon by neurons was lower than that of AβO.

Fig 1: Internalization of AβO, AβF and AβSon in primary neurons of the rat hippocampus. Fig.1 Internalisation of AβO, AβF and AβSon in primary hippocampal rat neurons.1

The cells were further tested for cell death rate at different time points. The results showed that AβO was toxic to cells only after 24 hours of incubation, when intracellular AβO levels increased.

Fig 2: The present study investigates the relationship between the internalization of AβO and its subsequent effect on cellular viability. Fig.2 Cytotoxicity of internalised AβO.1

In addition to the aforementioned assays, we offer customized services to meet your specific needs. Our Aβ induced toxicity assay service provides a comprehensive assessment of Aβ toxicity, facilitating the identification of potential therapeutic targets and drug screening. Please feel free to contact us to accelerate your research.

Reference

  1. Vadukul, Devkee M., et al. "Internalisation and toxicity of amyloid‐β 1‐42 are influenced by its conformation and assembly state rather than size." FEBS letters 594.21 (2020): 3490-3503. Distributed under Open Access license CC BY 4.0, without modification.
For Research Use Only. Not For Clinical Use.
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