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One of the initial pathological hallmarks of Alzheimer's disease is cognitive decline and
memory loss by disruption of cholinergic neurons and oxidative brain damage. A
postsynaptic muscarinic receptor blocker, scopolamine impairs cholinergic
transmission and impairs cognition. Here, we observed the physiological processes
underlying Saikosaponin b2's impact on memory deficits in mice that had been given
scopolamine repeatedly. Scopolamine (1 mg/kg) administration for 15 days caused
severe deficits in working and short-term memory in mice, as determined by the
elevated plus maze, Morris water maze, and novel object recognition tests. However,
scopolamine administered mice who were additionally given Saikosaponin b2 did not
experience either deficit. This effect was associated with an increase in antioxidant
enzymes (superoxide dismutase, Glutathione reductase, glutathione s transferase and
catalase), followed by reduction in lipid peroxidation and myeloperoxidase activity.