期刊
NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE
卷 17, 期 -, 页码 297-307出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.nano.2019.02.004
关键词
Alzheimer's disease; Amyloid beta; Neuronal loss; Vitamin D binding protein; PLGA; 5XFAD mice
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF)
- Ministry of Science, ICT, & Future Planning [NRF-2015R1C1A1A01052732, NRF-2018R1D1A3B07041059, NRF-2016R1C1B1015811]
- Cooperative Research Program for Agriculture Science and Technology Development Rural Development Administration, Republic of Korea [PJ01319901, PJ01428603]
The aggregation and accumulation of amyloid beta (A beta) peptide is believed to be the primary cause of Alzheimer's disease (AD) pathogenesis. Vitamin D-binding protein (DBP) can attenuate A beta aggregation and accumulation. A biocompatible polymer poly ((D,L)-lactic acid-co-glycolic acid) (PLGA) can be loaded with therapeutic agents and control the rate of their release. In the present study, a PLGA-based drug delivery system was used to examine the therapeutic effects of DBP-PLGA nanoparticles in A beta-overexpressing (5XFAD) mice. DBP was loaded into PLGA nanoparticles and the characteristics of the DBP-PLGA nanoparticles were analyzed. Using a thioflavin-T assay, we observed that DBP-PLGA nanoparticles significantly inhibited A beta aggregation in vitro. In addition, we found that intravenous injection of DBP-PLGA nanoparticles significantly attenuated the A beta accumulation, neuroinflammation, neuronal loss and cognitive dysfunction in the 5XFAD mice. Collectively, our results suggest that DBP-PLGA nanoparticles could be a promising therapeutic candidate for the treatment of AD. (C) 2019 Elsevier Inc. All rights reserved.
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