Protective effects of Glycyrrhiza uralensis Fisch.  on the cognitive deficits caused by beta-amyloid peptide 25-35 in young mice. 
Amyloid beta protein (Abeta) may be involved in the progression of Alzheimer's disease (AD), by acting as a neurotoxin and eliciting oxidative stress.  This study was designed to determine the effects of Glycyrrhiza uralensis Fisch.  water extract (GWE) on the cognitive deficits and oxidative stress induced by the administration of Abeta(25-35) in mice.  Mice in two of the four animal groups were fed an experimental diet containing either 0.5 or 1% GWE for the entire 6-week experimental period.  Control mice and a further experimental group were fed a non-GWE diet.  Abeta(25-35) was administered to the three experimental groups by intracerebroventricular (i.c.v.)  injection (10 microg/10 microl/mouse) once per week in weeks 5 and 6 of the experimental period.  Behavioral changes were assessed using both a passive avoidance (after the injection of Abeta(25-35) in week 5) and the Morris water-maze tests (after the injection of Abeta(25-35) in week 6).  Control animals were administered vehicle alone.  The prolonged consumption of a diet containing GWE ameliorated the cognitive deficits caused by the i.c.v.  injections of Abeta(25-35).  Treatment with Abeta(25-35) led to higher concentrations of thiobarbituric acid reactive substances in the brain, and GWE attenuated this response.  There was a decrease in catalase activity in the group provided with 1% GWE.  Acetylcholinesterase activity was significantly reduced in the brains of all GWE-treated animals compared to that in the non-GWE-fed experimental group.  These results suggest that GWE exerts a protective effect against the cognitive impairments often observed in AD, and that in mice this effect is mediated by antioxidant actions against oxidative stress.