Heat Shock Protein 70 in Alzheimer’s Disease

Author:

Lu Rui-Chun1,Tan Meng-Shan2,Wang Hao3,Xie An-Mu4,Yu Jin-Tai12ORCID,Tan Lan12ORCID

Affiliation:

1. Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No. 5 Donghai Middle Road, Qingdao 266071, China

2. Department of Neurology, Qingdao Municipal Hospital, College of Medicine and Pharmaceutics, Ocean University of China, Qingdao 266003, China

3. Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China

4. Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao 266000, China

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disease that caused dementia which has no effective treatment. Growing evidence has demonstrated that AD is a “protein misfolding disorder” that exhibits common features of misfolded, aggregation-prone proteins and selective cell loss in the mature nervous system. Heat shock protein 70 (HSP70) attracts extensive attention worldwide, because it plays a crucial role in preventing protein misfolding and inhibiting aggregation and represents a class of proteins potentially involved in AD pathogenesis. Numerous studies have indicated that HSP70 could suppress the progression of AD within vitroandin vivoexperiments. Thus, targeting HSP70 and the related compounds might represent a promising strategy for the treatment of AD.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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