%0 Journal Article
%T A combination extract of ginseng, epimedium, polygala, and tuber curcumae increases synaptophysin expression in APPV717I transgenic mice
%A Jing Shi
%A Jinzhou Tian
%A Xuekai Zhang
%A Mingqing Wei
%A Long Yin
%A Pengwen Wang
%A Yongyan Wang
%J Chinese Medicine
%D 2012
%I BioMed Central
%R 10.1186/1749-8546-7-13
%X Three-month-old APPV717I mice were arbitrarily divided into 10 groups (n£¿=£¿12 per group): APP groups receiving vehicle treatment for four or eight months (model groups), three dose groups of GEPT-treated mice for each treatment period, and donepezil-treated mice for each treatment period. Three-month-old C57BL/6£¿J mice (n£¿=£¿12) were also given vehicle for four or eight months (control groups). Vehicle, donepezil or GEPT were intragastrically administered. Immunohistochemistry (IHC) and Western blot analysis were used to assess protein expression in the hippocampal CA1 region and ratios of SYP to ¦Â-actin levels in hippocampal tissue homogenate, respectively.Both IHC and Western blot revealed a decrease in SYP levels in the CA1 region of 7- and 11-month-old APPV717I transgenic mice compared with the control groups, whereas SYP levels were increased in donepezil- and GEPT-treated transgenic mice compared with the APP group. There was a significant difference in the levels of SYP detected by IHC between the GEPT high-dose group and the APP group after 4£¿months of treatment, and there were significant differences between all three GEPT groups and the APP group after 8£¿months of treatment. Western blotting showed that the SYP protein¨C¦Â-actin ratio was decreased in APP mice, while donepezil- and GEPT-treated transgenic mice showed increased trends in the SYP protein¨C¦Â-actin ratios.GEPT increases SYP expression and protects synapses before and after the formation of amyloid plaques in the brains of APPV717I transgenic mice.Alzheimer¡¯s disease (AD), the most common cause of dementia in the elderly, currently affects about 26 million patients worldwide [1]. It is characterized clinically by a progressive impairment of cognitive functions, such as learning and memory, and pathologically by the accumulation of ¦Â-amyloid peptides (A¦Â), neurofibrillary tangles (NFTs) and neuronal degeneration [2]. Although A¦Â accumulation in neurons plays an important role in AD pathogenesis [3,4
%U http://www.cmjournal.org/content/7/1/13