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Curcumin could reduce the monomer of TTR with Tyr114Cys mutation via autophagy in cell model of familial amyloid polyneuropathy

Authors Li H, Zhang Y, Cao L, Xiong R, Zhang B, Wu L, Zhao Z, Chen SD

Received 9 July 2014

Accepted for publication 16 August 2014

Published 31 October 2014 Volume 2014:8 Pages 2121—2128

DOI https://doi.org/10.2147/DDDT.S70866

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 5

Editor who approved publication: Professor Shu-Feng Zhou

Hui Li,1,* Yu Zhang,1,* Li Cao,1 Ran Xiong,1 Bei Zhang,1 Li Wu,1 Zongbo Zhao,1 Sheng-Di Chen1,2

1Department of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 2Key Laboratory of Stem Cell Biology and Laboratory of Neurodegenerative Diseases, Institute of Health Science, Shanghai Institutes of Biological Sciences, Chinese Academy of Science, and Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China

*These authors contributed equally to this work


Abstract: Transthyretin (TTR) familial amyloid polyneuropathy (FAP) is an autosomal ­dominant inherited neurodegenerative disorder caused by various mutations in the transthyretin gene. We aimed to identify the mechanisms underlying TTR FAP with Tyr114Cys (Y114C) mutation. Our study showed that TTR Y114C mutation led to an increase in monomeric TTR and impaired autophagy. Treatment with curcumin resulted in a significant decrease of monomeric TTR by recovering autophagy. Our research suggests that impairment of autophagy might be involved in the pathogenesis of TTR FAP with Y114C mutation, and curcumin might be a potential therapeutic approach for TTR FAP.

Keywords: curcumin, familial amyloid polyneuropathy, transthyretin, autophagy

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