Toxic Amyloid-beta Peptide 1-42 Exposure Assay Service

At Creative Biolabs, we provide high-quality toxic amyloid-beta peptide (Aβ) 1-42 exposure assay services to help researchers gain a deeper understanding of the mechanism of action of Aβ1-42 in Alzheimer's disease (AD) and promote scientific research and technological progress in related fields. For more information on the products and services provided, project-specific consultations, and pricing, please submit an inquiry here.

Introduction

Available Assays at Creative Biolabs

• Cell Models

The SH-SY5Y human neuroblastoma cell line is frequently utilized in studies of Aβ1-42 toxicity. These cells exhibit heightened sensitivity to Aβ1-42 due to their absence of long nerve fibers and vulnerability to fibrosis.

Fig.1 Neuroblastoma SH-SY5Y cell line treated with Aβ1–42.^{2, 4}

• Proteomic Analysis

Liquid chromatography-tandem mass spectrometry (LC-MS/MS) technology has been employed to detect and quantify proteomic changes subsequent to Aβ1-42 treatment, thereby elucidating its effects on cellular protein expression.

• Drug Screening

Our scientific team is developing a variety of strategies to intervene in the toxic effects of Aβ1-42, including the use of small molecules, antibodies and gene editing technology. For example, inhibiting the aggregation of Aβ1-42 or altering its conformation may reduce its neurotoxicity.

Downstream Readouts

• Neuronal Death Assay

Aβ1-42 can induce apoptosis and necrosis in SH-SY5Y cells. Aβ1-42 has obvious toxic effects on neurons, resulting in decreased cell viability, morphological abnormalities (such as nuclear and membrane rupture), and reduced neurite length. We offer a range of readouts and assays around neuronal death.

Fig.2 Cell death and neurite retraction are induced by Aβ1-42.^{2, 4}

• Inflammatory Alterations

Aβ1-42 can activate inflammatory pathways, such as promoting inflammatory responses by upregulating the expression of TNFα and IL-1β. In addition, Aβ1-42 can increase the activation of microglia, further exacerbating the inflammatory response. We have several readouts available, including standard methods such as Western blot, ELISA and qPCR.

Fig.3 BV2 cells were treated with various doses of Aβ1-42.^{3, 4}

• Oxidative Stress and Autophagy

Aβ1-42 exposure induces oxidative stress, leading to elevated levels of reactive oxygen species (ROS) that impair cellular function. Aβ1-42 can also mitigate its toxic effects by activating autophagic pathways, such as PINK1/Parkin-mediated mitophagy.

• Custom assays

Our customized exposure assay service for Aβ1-42 utilizes advanced detection technology to precisely assess the toxic effects of Aβ1-42 on neural cells. This service empowers researchers to gain a more profound understanding of its role in the pathogenesis of AD. To obtain highly sensitive and specific test results that provide substantial support for your research, please contact us.

References

1. Zaretsky, Dmitry V., et al. "Patients with Alzheimer’s disease have an increased removal rate of soluble beta-amyloid-42." PLoS One 17.10 (2022): e0276933.
2. Thammasart, Siriluk, et al. "Attenuation Aβ1-42-induced neurotoxicity in neuronal cell by 660nm and 810nm LED light irradiation." PLoS One 18.7 (2023): e0283976.
3. Zhao, Xia, et al. "Artemisinin attenuates amyloid-induced brain inflammation and memory impairments by modulating TLR4/NF-κB signaling." International journal of molecular sciences 23.11 (2022): 6354.
4. Distributed under Open Access license CC BY 4.0, without modification.