ALZHEIMER DISEASE – Aβ42

Alzheimer’s (AD) is a type of dementia that affects memory, thinking and behavior. AD has no cure and is at the forefront of biomedical research today. AD is cause by hippocampal and cortical neurons degeneration. Their degeneration result in part from abnormal aggregation of Aβ42, key peptide involved in AD. Currently, scientists still do not know what causes the aggregation of Aβ42 and its mechanism on hippocampal and cortical neurons.

We have developed at NETRI compartmentalized microfluidic device architectures, with an enhanced fluidic isolation, to understand the causes of Aβ42 aggregation and its mode of action in AD.

-                                        CAPABILITIES
+                                        Co-culture,

 hiPSC Derived Cell, 

 Readouts
-                                        CHIP
+                                        DuaLink
-                                        CELL TYPE
+                                        Glutamatergic Neurons
-                                        RESOURCES
+                                        Publications,



Application Note,


Application Protocol,


Posters,


Cells DataSheet
+                                        (FujiFilm CDI, BrainXell),
Chip DataSheet
-                                        RELATED PAPERS
+                                        Deleglise, B., Magnifico, S., Duplus, E., Vaur, P., Soubeyre, V., Belle, M., Vignes, M., Viovy, J. L., Jacotot, E., Peyrin, J. M., & Brugg, B. (2014). Β-Amyloid Induces a Dying-Back Process and Remote Trans-Synaptic Alterations in a Microfluidic-Based Reconstructed Neuronal Network. Acta Neuropathologica Communications, 2(1), 1–9.
+Lee, J. S., & Park, C. B. (2010). Microfluidic dissociation and clearance of Alzheimer’s β-amyloid aggregates. Biomaterials, 31(26), 6789–6795. 



Cho, H., Hashimoto, T., Wong, E., Hori, Y., Wood, L. B., Zhao, L., Haigis, K. M., Hyman, B. T., & Irimia, D. (2013). Microfluidic chemotaxis platform for differentiating the roles of soluble and bound amyloid-β on microglial accumulation. Scientific Reports, 3, 1–7. 



Ruiz, A., Joshi, P., Mastrangelo, R., Francolini, M., Verderio, C., & Matteoli, M. (2014). Testing Aβ toxicity on primary CNS cultures using drug-screening microfluidic chips. Lab on a Chip, 14(15), 2860–2866.






Park, J., Wetzel, I., Marriott, I., Dréau, D., D’Avanzo, C., Kim, D. Y., Tanzi, R. E., & Cho, H. (2018). A 3D human triculture system modeling neurodegeneration and neuroinflammation in Alzheimer’s disease. Nature Neuroscience, 21(7), 941–951. 



Poon, W. W., Blurton-Jones, M., Tu, C. H., Feinberg, L. M., Chabrier, M. A., Harris, J. W., Jeon, N. L., & Cotman, C. W. (2011). β-Amyloid impairs axonal BDNF retrograde trafficking. Neurobiology of Aging, 32(5), 821–833. 



Song, H. L., Shim, S., Kim, D. H., Won, S. H., Joo, S., Kim, S., Jeon, N. L., & Yoon, S. Y. (2014). β-Amyloid is transmitted via neuronal connections along axonal membranes. Annals of Neurology, 75(1), 88–97. 



Li, W., Xu, Z., Xu, B., Chan, C. Y., Lin, X., Wang, Y., & Chen, G. (2017). Investigation of the Subcellular Neurotoxicity of Amyloid- β Using a Device Integrating Microfluidic Perfusion and Chemotactic Guidance. 201600895, 1–8.



Kilinc, D., Vreulx, A.-C., Mendes, T., Flaig, A., Marques-Coelho, D., Verschoore, M., Demiautte, F., Amouyel, P., Eysert, F., Dourlen, P., Chapuis, J., Costa, M. R., Malmanche, N., Checler, F., & Lambert, J.-C. (2019). Pyk2 Overexpression in Postsynaptic Neurons Blocks Aβ 1-42 -induced Synaptotoxicity in a Microfluidic Co-Culture Model. 2020. 



Brahic, M., Bousset, L., Bieri, G., Melki, R., & Gitler, A. D. (2016). Axonal transport and secretion of fibrillar forms of α-synuclein, Aβ42 peptide and HTTExon 1. Acta Neuropathologica, 131(4), 539–548.
-                                        READINESS LEVEL
+                                        Protocol ⑤ / ⑧ Cell alteration done

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ALZHEIMER DISEASE – Aβ42

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