Affiliations: [a] Department of Oriental Neuropsychiatry, Graduate School of Oriental Medicine, Dongguk University, Goyang, Republic of Korea
| [b] Woobo Research Institute of Oriental Medicine Co. Ltd, Seoul, Republic of Korea
| [c] Department of Neuropsychiatry, Dongguk University Bundang Oriental Hospital, Seongnam, Republic of Korea
| [d] Department of Biomedical Sciences, Center for Glocal Future Biomedical Scientists at Chonnam National University, Gwangju, Republic of Korea
| [e] Department of Korean Neuropsychiatry, Dongguk University Ilsan Hospital, Goyang, Republic of Korea
Correspondence:
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Correspondence to: Songhee Jeon, PhD, Department of Biomedical Sciences, Center for Glocal Future Biomedical Scientists at Chonnam National University, Gwangju, 61469, Republic of Korea. Tel.: +82 61 379 2862; Fax: +82 61 379 2753; E-mail: jsong0304@jnu.ac.kr; Byung-Soo Koo, OMD, PhD, Department of Korean Neuropsychiatry, Dongguk University Ilsan Oriental Hospital, Goyang, Republic of Korea. Tel.: +82 31 961 0001; Fax: +82 31 961 9009; E-mail: koobs@dongguk.ac.kr.
Abstract: Background:Alzheimer’s disease (AD) is the most general, chronic, and progressive neurodegenerative senile disorder characterized clinically by progressive cognitive deterioration and memory impairment. Neoline is effective against neuropathic pain models, but the effects of neoline against AD-like phenotypes have not been investigated. Objective:We offer the investigation of the effects of neoline in AD. Methods:In this study, a Tg-APPswe/PS1dE9 AD mouse model was treated orally with neoline at a concentration of 0.5 mg/kg or 0.1 mg/kg starting at 7.5 months and administered for three months, and its anti-AD effects were evaluated. Results:Neoline improved memory and cognition impairments and reduced the number of amyloid-beta plaque and the amount of amyloid-β in the brain of AD mice. Furthermore, neoline reduced the anxiety behavior in the AD mouse model. The chronic administration of neoline also induced AMPK phosphorylation and decreased tau, amyloid-β, and BACE1 expression in the hippocampus. These findings indicate that chronic administration of neoline has therapeutic effects via AMPK activation, and BACE1 downregulation resulted in a decrease in the amyloid-β levels in the brain of Tg-APPswe/PS1dE9 AD mice. Conclusion:Our results suggest that neoline is a therapeutic agent for the cure of neurodegenerative diseases like AD.
Keywords: Alzheimer’s disease, AMPK, BACE1, cognitive function, neoline, tau
