Aβ Induced Neurotoxicity Assay

Amyloid beta (Aβ or Abeta) is the main component of the senile plaques which is considered as one of the major pathological hallmarks of Alzheimer's disease (AD). Aβ presents in different assembly forms including monomers, oligomers, and fibrils. Among them, Aβ oligomers were shown to play a crucial role in neurotoxicity associated with the progression of AD. In which, Aβ_1-42 oligomers seem to be more toxic than Aβ_1-40, and exhibit a higher propensity to form fibrils in vitro.

Figure 1 Aβ neurotoxicity. Administration of 5 μM oligomeric Aβ (oAβ₄₂) to cortical cultures induces significant neuronal death. In contrast, administration of fibrillar Aβ (fAβ₄₂) does not induce neuronal cell death, although Aβ deposition is observed on dendrites.

Figure 2 Aβ toxicity in neurons and microglia

Aβ_1-42 oligomers-induced neurotoxicity in primary neurons or several cell lines is an important AD in vitro model. Creative Bioarray offers development of custom designed in vitro models by using primary neuronal cultures, cell lines, iPS cells with genetic modifications, which are phenotypically closer to the adult neuronal network and mimic the development of AD. These in vitro models are capable of providing a rapid screening of the neuroprotective potential agents for the treatment of AD.

We provide this powerful and versatile tool for developing AD therapy as well as basic research to help our customers understand more about the underlying mechanisms of the progression of AD.

Study Examples

Figure 3 Compound 30 alleviates Aβ₄₂ induced neurotoxicity in SH-SY5Y cells.

Figure 4 Salidroside (sal) inhibits Aβ-induced neurotoxicity by activating the Akt/mTOR/p70S6K pathway in primary cultured cortical neurons.

Figure 5 Aβ induced synapse damage in human iPSC-derived cortical neurons.

Figure 6 Linagliptin reduces Aβ-induced intracellular ROS accumulation and improves mitochondria dysfunction.

Quotation and ordering

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References

1. Mizuno T. The biphasic role of microglia in Alzheimer's disease. International Journal of Alzheimer's Disease. 2012, 2012: 1-09.
2. Liang Z, Li QX. Discovery of selective, substrate-competitive, and passive membrane permeable glycogen synthase kinase-3β inhibitors: synthesis, biological evaluation, and molecular modeling of new C-glycosylflavones. ACS Chem Neurosci. 2018, 9(5): 1166-1183.
3. Chen S.; et al. Neuroprotective effects of salidroside through PI3K/Akt pathway activation in Alzheimer’s disease models. Drug Design, Development and Therapy. 2016(10): 1335-1343.
4. Nieweg K.; et al. Alzheimer's disease-related amyloid-β induces synaptotoxicity in human iPS cell-derived neurons. Cell Death Dis. 2015, 6(4): e1709.
5. Kornelius E.; et al. DPP-4 inhibitor linagliptin attenuates Aβ-induced cytotoxicity through activation of AMPK in neuronal cells. CNS Neurosci Ther. 2015, 21(7): 549-557.

For research use only. Not for any other purpose.