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Jung YY, Lee YJ, Choi DY, et al. Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol. Biomol Ther (Seoul). 2014;22(3):232-8doi: 10.4062/biomolther.2014.030.
Jung, Y. Y., Lee, Y. J., Choi, D. Y., & Hong, J. T. (2014). Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol. Biomolecules & therapeutics, 22(3), 232-8. https://doi.org/10.4062/biomolther.2014.030
Jung, Yu-Yeon, et al. "Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol." Biomolecules & therapeutics vol. 22,3 (2014): 232-8. doi: https://doi.org/10.4062/biomolther.2014.030
Jung YY, Lee YJ, Choi DY, Hong JT. Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol. Biomol Ther (Seoul). 2014 May;22(3):232-8. doi: 10.4062/biomolther.2014.030. PMID: 25009704; PMCID: PMC4060074.
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Biomol Ther (Seoul). 2014 May;22(3):232-8. doi: 10.4062/biomolther.2014.030.

Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol.

Biomolecules & therapeutics

Yu-Yeon Jung, Young-Jung Lee, Dong-Young Choi, Jin Tae Hong

Affiliations

  1. College of Pharmacy, Chungbuk National University, Cheongju 361-763.
  2. School of Equine industries, Cheju Halla University, Jeju 690-708.
  3. College of Pharmacy, Yeungnam University, Gyeongsan 712-749, Republic of Korea.

PMID: 25009704 PMCID: PMC4060074 DOI: 10.4062/biomolther.2014.030

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease without known ways to cure. A key neuropathologic manifestation of the disease is extracellular deposition of beta-amyloid peptide (Aβ). Specific mechanisms underlying the development of the disease have not yet been fully understood. In this study, we investigated effects of 4-O-methylhonokiol on memory dysfunction in APP/PS1 double transgenic mice. 4-O-methylhonokiol (1 mg/kg for 3 month) significantly reduced deficit in learning and memory of the transgenic mice, as determined by the Morris water maze test and step-through passive avoidance test. Our biochemical analysis suggested that 4-O-methylhonokiol ameliorated Aβ accumulation in the cortex and hippocampus via reduction in beta-site APP-cleaving enzyme 1 expression. In addition, 4-O-methylhonokiol attenuated lipid peroxidation and elevated glutathione peroxidase activity in the double transgenic mice brains. Thus, suppressive effects of 4-O-methylhonokiol on Aβ generation and oxidative stress in the brains of transgenic mice may be responsible for the enhancement in cognitive function. These results suggest that the natural compound has potential to intervene memory deficit and progressive neurodegeneration in AD patients.

Keywords: 4-O-methylhonokiol; APP/PS1 double transgenic; Alzheimer’s disease; Antioxidant; Beta-site APP-cleaving enzyme

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