| Literature DB >> 26358038 |
Juanfang Liu1,2, Xiaodong Yan3, Ling Li4, Yuan Li5, Linfu Zhou1, Xiaohui Zhang1, Xinghua Hu6, Gang Zhao7.
Abstract
Alzheimer's disease (AD) is a complicated neurodegenerative disease which causes memory loss and dementia. Many researchers have revealed the vital roles of β-amyloid proteins (Aβ) in the proceeds of AD. Aβ deposition in AD patients' brains might function as immune stimulus, and inflammation is believed to play an important role in AD pathologically. We experimentally used amyloid β-protein precursor (APP) transgenic (Tg) mice in this study to further clarify the neuroprotective effects of ginsenoside Rd on AD and its possible mechanisms. It was found that Rd could improve learning and memory ability in APP Tg mice, probably through inhibiting the transcription activity of NFκB. With the activation of the NFκB pathway being suppressed, the reduction of pro-inflammatory cytokines and the generation of protective factors had been increased ultimately. In conclusion, Rd had a neuroprotective effect on APP Tg mice, and it can be used as an alternative drug therapy in AD patients for their memory dysfunction.Entities:
Keywords: APP transgenic mice; Alzheimer’s disease; Ginsenoside Rd; Inflammatory reaction
Mesh:
Substances:
Year: 2015 PMID: 26358038 DOI: 10.1007/s12031-015-0632-4
Source DB: PubMed Journal: J Mol Neurosci ISSN: 0895-8696 Impact factor: 3.444