Abstract
Aggregation of Alzheimer’s amyloid-β peptide (Aβ) and formation of amyloid plaques and vascular amyloid are considered a cause of dementia of the Alzheimer’s type. The mechanisms and/or agents that trigger fibrillization of Aβ, which could be the targets of rational therapy for Alzheimer’s disease (AD), are still unknown. The lack of appropriate experimental models has restricted the search for potential anti-β-amyloidogenic drugs and the development of treatment procedures. In the present study, we demonstrated the cellular model of β-amyloidogenesis, which appears to possess various features of the in vivo pathology and could be useful for drug evaluation. We also used cell-free in vitro methods to examine the ability of various factors to interfere with aggregation and fibrillization of synthetic Aβ.
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© 1997 Birkhäuser Boston
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Wisniewski, H.M., Frackowiak, J., Mazur-Kolecka, B., Wegiel, J., Chauhan, A., Chauhan, V.P.S. (1997). Cellular and Test Tube Models of Amyloid-βFormation. In: Becker, R.E., Giacobini, E., Barton, J.M., Brown, M. (eds) Alzheimer Disease. Advances in Alzheimer Disease Therapy. Birkhäuser Boston. https://doi.org/10.1007/978-1-4612-4116-4_12
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DOI: https://doi.org/10.1007/978-1-4612-4116-4_12
Publisher Name: Birkhäuser Boston
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