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

Title
Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol
Author(s)
최동영정유연[정유연]이영중[이영중]홍진태[홍진태]
Keywords
AMYLOID PRECURSOR PROTEIN; GAMMA-SECRETASE ACTIVITY; ALZHEIMERS-DISEASE; MEMORY IMPAIRMENT; BETA-SECRETASE; OXIDATIVE STRESS; MAGNOLIA-OFFICINALIS; MUTANT PRESENILIN-1; MOUSE MODEL; KAPPA-B
Issue Date
201405
Publisher
KOREAN SOC APPLIED PHARMACOLOGY
Citation
BIOMOLECULES & THERAPEUTICS, v.22, no.3, pp.232 - 238
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 (A beta). 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 A beta 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 A beta 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.
URI
http://hdl.handle.net/YU.REPOSITORY/32178http://dx.doi.org/10.4062/biomolther.2014.030
ISSN
1976-9148
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약학대학 > 약학부 > Articles
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