期刊
BRAIN RESEARCH
卷 1529, 期 -, 页码 113-124出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2013.05.045
关键词
Alzheimer's disease model; Amyloid-beta; Recombinant soluble neprilysin; Protein delivery
资金
- Bio & Medical Technology Development Program of the National Research Foundation (NRF) of Korea [2010-0020234, 2012M3A9C6049913]
- Basic Science Research Program of the National Research Foundation (NRF) of Korea [2010-0009421]
- Conversing Research Center Program of the National Research Foundation (NRF) of Korea [2009-0081959]
- Ministry of Education, Science and Technology, Republic of Korea
- National Research Foundation of Korea [2009-0081959, 2010-0020234, 2010-0009421, 2012M3A9C6049913] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Accumulation of amyloid-beta (A beta) is thought to be a central pathology in the brain of patients with Alzheimer's disease (AD). Neprilysin (NEP), a plasma membrane glycoprotein of the neutral zinc metalloendopeptidase family, is known as a major A beta-degrading enzyme in the brain. The level of NEP is reduced in the brains of patients with AD; therefore, NEP is under intense investigation as a potential therapeutic source for degradation of deposited A beta in AD. Previous studies have utilized viral vectors expressing NEP for reduction of A beta deposition in the brain. However, viral vectors have disadvantages regarding difficulty in control of insert size, expression desired (short- or long-term), and target cell type. Here, in order to overcome these disadvantages, we produced recombinant soluble NEP from insect cells using an NEP expression vector, which was administered by intracerebral injection into AD mice, resulting in significantly reduced accumulation of A beta. In addition, AD mice treated with NEP showed improved behavioral performance on the water maze test. These data support a role of recombinant soluble NEP in improving memory impairment by regulation of A beta deposition and suggest the possibility that approaches using protein therapy might have potential for development of alternative therapies for treatment of AD. (C) 2013 Elsevier B.V. All rights reserved.
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