A metabonomic method was established to find potential
biomarkers and study the metabolism disturbance in
Alzheimer disease animal model. Total
ginsenosides, as potential agent in neuroprotection and anti-
inflammation, was also studied to learn the regulation mechanism to plasma metabolites in model animals. In experiment,
amyloid beta 1-42 was occupied to form
Alzheimer disease animal model. After
drug administration, animals were evaluated by Morris water maze behavior test and sacrificed. Plasma samples were then analyzed using UHPLC-TOF/MS method to determine the endogenous metabolites. Behavior test results revealed that the spatial learning and memory abilities were deficit in model mice, and total
ginsenosides could improve cognition abilities in dose-dependent manners. Principal component analysis showed that model and
sham were divided into two groups, which means the metabolic network of mice was disturbed after modeling. Accordingly, 19
biomarkers were found and identified. In model group, the levels of
proline,
valine,
tryptophan, LPC (14:0), LPC (15:0), LPC (15:1), LPC (17:0), LPC (18:2), LPC (18:3) and LPC (20:4) were up-regulated, while the levels of
acetylcarnitine,
palmitoylcarnitine, vaccenylcarnitine,
phytosphingosine, N-eicosanoylethanolamine,
hexadecenoic acid,
docosahexaenoic acid,
docosapentaenoic acid and
octadecadienoic acid were down-regulated. The levels of these metabolites were recovered in different degrees after total
ginsenosides administration. Combining with behavior study results, total
ginsenosides could ameliorate both cognition symptoms and metabolic changes in model animals. This metabonomic approach provided a feasible way to understand the endogenous alterations of AD and to study the pharmacodynamic activity of novel agents.