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dc.contributor.authorFang, Fang
dc.contributor.authorChen, Xiaochun
dc.contributor.authorHuang, Tianwen
dc.contributor.authorLue, Lih-Fen
dc.contributor.authorLuddy, John S.
dc.contributor.authorYan, Shirley ShiDu
dc.date.accessioned2017-02-15T18:15:38Z
dc.date.available2017-02-15T18:15:38Z
dc.date.issued2011-10-12
dc.identifier.citationFang, F., Chen, X., Huang, T., Lue, L. F., Luddy, J. S., & Yan, S. S. (2012). Multi-faced neuroprotective effects of Ginsenoside Rg1 in an Alzheimer mouse model. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1822(2), 286-292.en_US
dc.identifier.urihttp://hdl.handle.net/1808/23179
dc.description.abstractThere has been no extensive characterization of the effects of Ginsenoside Rg1, a pharmacological active component purified from the nature product ginseng, in an Alzheimer's disease mouse model. The well-characterized transgenic Alzheimer disease (AD) mice over expressing amyloid precursor protein (APP)/Aβ (Tg mAPP) and nontransgenic (nonTg) littermates at age of 6 and 9 months were treated with Rg 1 for three months via intraperitoneal injection. Mice were then evaluated for changes in amyloid pathology, neuropathology and behavior. Tg mAPP treated with Rg1 showed a significant reduction of cerebral Aβ levels, reversal of certain neuropathological changes, and preservation of spatial learning and memory, as compared to vehicle-treated mice. Rg1 treatment inhibited activity of γ-secretase in both Tg mAPP mice and B103-APP cells, indicating the involvement of Rg1 in APP regulation pathway. Furthermore, administration of Rg1 enhanced PKA/CREB pathway activation in mAPP mice and in cultured cortical neurons exposed to Aβ or glutamate-mediated synaptic stress. Most importantly, the beneficial effects on attenuation of cerebral Aβ accumulation, improvement in neuropathological and behavioral changes can be extended to the aged mAPP mice, even to 12–13 months old mice that had extensive amyloid pathology and severe neuropathological and cognitive malfunction. These studies indicate that Rg1 has profound multi-faced and neuroprotective effects in an AD mouse model. Rg1 induces neuroprotection through ameliorating amyloid pathology, modulating APP process, improving cognition, and activating PKA/CREB signaling. These findings provide a new perspective for the treatment of AD and demonstrate potential for a new class of drugs for AD treatment.en_US
dc.publisherElsevieren_US
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectRg1en_US
dc.subjectAD mouse modelen_US
dc.subjectNeuroprotectionen_US
dc.subjectGamma secretaseen_US
dc.titleMulti-faced neuroprotectice effects of Ginsenoside Rg1 in an Alzheimer mouse modelen_US
dc.typeArticleen_US
kusw.kuauthorYan, Shirley ShiDu
kusw.kudepartmentHiguchi Biosciences Centeren_US
dc.identifier.doi10.1016/j.bbadis.2011.10.004en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccess


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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.