s-allylcysteine and Memory-Disorders

This study examined the effect of S:-allylcysteine (SAC), a major thioallyl compound found in aged garlic extract, on the memory deficit and age-related changes of senescence-accelerated mice. Senescence-accelerated prone P8 mice fed a diet supplemented with 40 mg SAC/kg diet for 8 mo had a significantly attenuated decrease in the conditioned avoidance response compared with those not given SAC. In the elevated plus-maze test using senescence-accelerated prone P10 mice, the percentage of time spent on the open arm was greater compared with the senescence-resistant control mice. Chronic dietary treatment with 40 mg SAC/kg diet decreased the time in the open arm in senescence-accelerated prone P10 mice. These studies suggest that diet supplementation with SAC may reduce age-related learning disabilities and cognitive disorders in senescence-accelerated mice.

Topics: Aging; Animals; Avoidance Learning; Body Weight; Cysteine; Garlic; Male; Maze Learning; Memory Disorders; Mice; Phytotherapy; Plant Extracts; Plants, Medicinal

The efficacy of S-allylcysteine (SAC) as a free radical scavenger was studied using rat brain ischemia models. In a middle cerebral artery occlusion model, preischemic administration of SAC had the following effects: it improved motor performance and memory impairment and reduced water content and the infarct size. In a transient global ischemia model, the time course of free radical (alkoxyl radical) formation as studied by electron paramagnetic resonance (EPR) spectroscopy and alpha-phenyl-N-tert-butylnitrone (PBN) was biphasic; the first peak occurred at 5 min and the second at 20 min after reperfusion. Although SAC did not attenuate the first peak, it did affect the second peak, which is related to lipid peroxidation. The lipid peroxidation as estimated by thiobarbituric acid reactive substances (TBARS) increased significantly at 20 min after reperfusion. SAC decreased TBARS to the levels found without ischemia. These results suggest that SAC could have beneficial effects in brain ischemia and that the major protective mechanism may be the inhibition of free radical-mediated lipid peroxidation.

Topics: Animals; Antioxidants; Cysteine; Disease Models, Animal; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Free Radicals; Ischemic Attack, Transient; Lipid Peroxidation; Male; Memory Disorders; Neurons; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Thiobarbituric Acid Reactive Substances; Time Factors; Water