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Publication : YXQN Reduces Alzheimer's Disease-Like Pathology and Cognitive Decline in APPswePS1dE9 Transgenic Mice.

First Author  Wang X Year  2017
Journal  Front Aging Neurosci Volume  9
Pages  157 PubMed ID  28603494
Mgi Jnum  J:275603 Mgi Id  MGI:6307664
Doi  10.3389/fnagi.2017.00157 Citation  Wang X, et al. (2017) YXQN Reduces Alzheimer's Disease-Like Pathology and Cognitive Decline in APPswePS1dE9 Transgenic Mice. Front Aging Neurosci 9:157
abstractText  Alzheimer's disease (AD) is the world's most common form of dementia, in which aggregation of amyloid-beta (Abeta) is the hallmark. Unfortunately, few medicines have succeeded to completely cure AD. Yangxue Qingnao (YXQN) is a Chinese traditional medicine, and its pharmacological effect is improving cerebral blood flow. In this study, we firstly demonstrated that YXQN reduced AD-like pathology and cognitive impairment in APPswePS1dE9 (APP/PS1) mice with 2 months administration. Our data showed that YXQN substantially ameliorated behavioral defects in 10-month old APP/PS1 mice using Morris Water Maze and Y-maze tests, in which the cognitive ability of YXQN high-dose group approaches to wild type mice. Next, we focused on the brain pathological alterations in the YXQN group by three experiments, including thioflavin-S, congo-red, and Abeta-immunohistochemistry staining. The results demonstrated that the high-dose of YXQN dramatically suppressed amyloid plaques in the hippocampus and cortex of APP/PS1 mice, which showed a 47-72% reduction in plaque deposits, relative to the vehicle group. In addition, our data verified that YXQN decreased the cerebral amyloid load by attenuating beta-secretase BACE1 and gamma-secretase PS1 in the pathological processing of APP, and promoting the level of alpha-secretase ADAM10 in the physiological processing of APP to generate more sAPPalpha, which combats amyloidosis formation, and also carries out neurotropic and neuroprotective effect. Taken together, our results strongly suggest that YXQN could be a potential medicine for AD, and provide new evidence for further AD drug research and development.
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