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Creative Biolabs

Amyloid-beta Induced Toxicity Assay

Alzheimer's disease (AD) is a common cognitive disorder. In recent years, scientific and clinical research on AD has been greatly expanded. The deleterious cascade induced by soluble amyloid-β (Aβ) is thought to be closely related to the pathology of AD. Therefore, exploring the role of toxic Aβ in the brain is beneficial for understanding the pathogenesis and treatment of AD. Creative Biolabs has built a comprehensive assay platform and developed multiple specific cell lines to assist your Aβ-induced toxicity assay related projects.

Background of Aβ

Numerous genetic and environmental factors, as well as aging, contribute to the pathology of AD. Aβ toxicity, tau hyperphosphorylation, apoptosis induction, and autophagy dysregulation are all associated with AD. Notably, neuroinflammation has received considerable attention as a common pathway for inducing many underlying pathologies of AD. Evidence accumulated over the past 20 years indicated that soluble Aβ oligomer (AβO) plaques trigger synaptic failure and memory impairment. Therefore, soluble AβO has received great attention in the analysis of AD pathogenesis.

Aβ physiological functions.Fig.1 Aβ physiological functions. (Rajasekhar, et al., 2015)

Aβ Toxicity and AD

It has been reported that overproduction of Aβ or its impaired clearance contributed to the initiation and progression of neuronal damage. Soluble oligomeric conformations of Aβ, which are toxic substances, are emerging as a research focus since these conformations are closely related to the severity of AD. Oligomeric forms of Aβ are highly toxic to the brain, causing synaptic dysfunction and neuronal damage. Scientists have identified many Aβ molecular species and found that all of them adversely affect memory formation in mice, so Aβ formation and accumulation in the brain was considered an important factor in AD. In addition, experiments have demonstrated that a wide range of toxicity mechanisms was related to Aβ, such as oxidative stress, mitochondrial changes, synaptic dysfunction, and excitotoxicity.

Aβ Induced Toxicity Assay

Aβ exists in different assembled forms. Among them, Aβ1-40 oligomers are neurotoxic, and Aβ1-42 oligomers show a higher tendency to form fibrils in vitro and are more neurotoxic. Intoxication of neurons by Aβ1-40 and Aβ1-42 oligomers is a potential in vitro modeling method for AD. These in vitro models enable rapid screening of drugs for inhibiting neuronal damage in AD. At Creative Biolabs, we provide a variety of conventional methods for assessing Aβ neurotoxicity, including but not limited to:

  • MTT assay
  • Propidium iodide (PI) assay
  • Lactate dehydrogenase assay
  • Trypan blue assay
  • TUNEL assay

In addition to these methods, we have also developed some novel assays, such as two-color assays, which are useful for the rapid detection of Aβ-induced cellular changes. Creative Biolabs is committed to providing customized Aβ-induced toxicity assay to help our clients gain insight into the underlying mechanisms of AD. If you have any difficulties in the project of Aβ-induced toxicity assay, please contact us for help in time.

Reference

  1. Rajasekhar, K.; et al. Function and toxicity of amyloid beta and recent therapeutic interventions targeting amyloid beta in Alzheimer's disease. Chemical communications. 2015, 51(70): 13434-13450.
For Research Use Only. Not For Clinical Use.
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