Effects of a Dehydroevodiamine-Derivative on Synaptic Destabilization and Memory Impairment in the 5xFAD, Alzheimer's Disease Mouse Model
- Authors
- Kang, Shinwoo; Ha, Sungji; Park, Hyunjun; Nam, Eunjoo; Suh, Won Hyuk; Suh, Yoo-Hun; Chang, Keun-A
- Issue Date
- 13-Nov-2018
- Publisher
- FRONTIERS MEDIA SA
- Keywords
- Alzheimer' s disease; carboxy-dehydroevodiamine; memory impairment; 5xFAD; synaptic destabilization
- Citation
- FRONTIERS IN BEHAVIORAL NEUROSCIENCE, v.12
- Journal Title
- FRONTIERS IN BEHAVIORAL NEUROSCIENCE
- Volume
- 12
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3085
- DOI
- 10.3389/fnbeh.2018.00273
- ISSN
- 1662-5153
- Abstract
- Carboxy-dehydroevodiamine-HCI (cx-DHED) is a derivative of DHED, which improves memory impairment. Carboxyl modification increases solubility in water, indicating that its bioavailability is higher than that of DHED. Cx-DHED is expected to have better therapeutic effects on Alzheimer's disease (AD) than DHED. In this study, we investigated the therapeutic effects of cx-DHED and the underlying mechanism in 5xFAD mice, transgenic (Tg) mouse model of AD model mice. In several behavioral tests, such as Y-maze, passive avoidance, and Morris water maze test, memory deficits improved significantly in cx-DHED-treated transgenic (Tg) mice compared with vehicle-treated Tg mice. We also found that AD-related pathologies, including amyloid plaque deposition and tau phosphorylation, were reduced after the treatment of Tg mice with cx-DHED. We determined the levels of synaptic proteins, such as GluN1, GluN2A, GluN2B, PSD-95 and Rabphilin3A, and Rab3A in the brains of mice of each group and found that GluN2A and PSD-95 were significantly increased in the brains of cx-DHED-treated Tg mice when compared with the brains of Tg-vehicle mice. These results suggest that cx-DHED has therapeutic effects on 5xFAD, AD model mice through the improvement of synaptic stabilization.
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