Taurine Prevents Passive Avoidance Memory Impairment, Accumulation of Amyloid-β Plaques, and Neuronal Loss in the Hippocampus of Scopolamine-Treated Rats

One of the hallmarks of Alzheimer's disease (AD) is extracellular deposition of amyloid-beta peptides, particularly in the hippocampus. Despite the antioxidant properties of taurine, its neuroprotective potential against amyloid-beta accumulation in scopolamine-induced AD model remain unclear. In such a model, we aimed to assess the effects of taurine on passive avoidance memory impairment, accumulation of congophilic amyloid-beta plaques, and neuronal density in the rat hippocampus. Rats, except the control group, were i.p. injected with 3 mg/kg scopolamine. The pretreated and treated groups were also injected with taurine (25, 50, or 100 mg/kg/day, i.p.) for 14 days before or after scopolamine introduction. All rats (except the control group) were tested for the passive avoidance reaction 24 h after the last drug injection. For histological analysis, hippocampal sections were stained with Congo red and cresyl violet. Administration of taurine for 14 days, both before and after scopolamine injection, significantly alleviated passive avoidance memory impairment. Pretreatment with taurine in any of the mentioned dosages significantly decreased the number of congophilic amyloid-beta plaques in the rat hippocampus, including the CA3 area. Taurine also reduced scopolamine-induced neuronal loss in the hippocampus.