Volume 8 Issue 1
Feb.  2022
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Long Houfang, Zeng Shuyi, Li Dan. Cellular and animal models to investigate pathogenesis of amyloid aggregation in neurodegenerative diseases[J]. Biophysics Reports, 2022, 8(1): 14-28. doi: 10.52601/bpr.2022.210033
Citation: Long Houfang, Zeng Shuyi, Li Dan. Cellular and animal models to investigate pathogenesis of amyloid aggregation in neurodegenerative diseases[J]. Biophysics Reports, 2022, 8(1): 14-28. doi: 10.52601/bpr.2022.210033

Cellular and animal models to investigate pathogenesis of amyloid aggregation in neurodegenerative diseases

doi: 10.52601/bpr.2022.210033
Funds:  This work was supported by the Major State Basic Research Development Program (2019YFE0120600), the National Natural Science Foundation (NSF) of China (91853113 and 31872716), the Science and Technology Commission of Shanghai Municipality (STCSM) (18JC1420500, 20XD1425000 and 2019SHZDZX02), the “Eastern Scholar” project supported by the Shanghai Municipal Education Commission. Figures are created with BioRender.com. We acknowledge the resources provided by this website. HL summarized the protocol; HL and SZ carried out the experiments which formed the protocol, HL analyzed data and prepared figures; and HL, SZ and DL wrote the manuscript. All authors read and approved the final manuscript.
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  • Corresponding author: lidan2017@sjtu.edu.cn
  • Received Date: 30 July 2021
  • Accepted Date: 27 September 2021
  • Available Online: 21 January 2022
  • Publish Date: 28 February 2022
  • Abnormal aggregation of amyloid proteins, e.g. amyloid β (Aβ), Tau and α-synuclein (α-syn), is closely associated with a variety of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Cellular and animal models are useful to explore the neuropathology of amyloid aggregates in disease initiation and progression. In this protocol, we describe detailed procedures for how to establish neuronal and PD mouse models to evaluate amyloid pathologies including self-propagation, cell-to-cell transmission, neurotoxicity, and impact on mouse motor and cognitive functions. We use α-syn, a key pathogenic protein in PD, as an example to demonstrate the application of the protocol, while it can be used to investigate the pathologies of other amyloid proteins as well. The established disease models are also useful to assess the activities of drug candidates for therapeutics of neurodegenerative diseases.
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