171 0090-2977/19/5103-00171 © 2019 Springer Science+Business Media LLC Neurophysiology, Vol. 51, No. 3, May, 2019 Taurine Prevents Passive Avoidance Memory Impairment, Accumulation of Amyloid-β Plaques, and Neuronal Loss in the Hippocampus of Scopolamine-Treated Rats S. Gorgani, 1 M. Jahanshahi, 1 and L. Elyasi 1 Received November 20, 2018 One of the hallmarks of Alzheimer’s disease (AD) is extracellular deposition of amyloid-β peptides, particularly in the hippocampus. Despite the antioxidant properties of taurine, its neuroprotective potential against amyloid-β 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-β 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-β plaques in the rat hippocampus, including the CA3 area. Taurine also reduced scopolamine-induced neuronal loss in the hippocampus. Keywords: Alzheimer’s disease (AD), scopolamine, hippocampus, amyloid-β (Aβ) plaques, neuronal density, avoidance reaction, taurine. 1 Neuroscience Research Center, Department of Anatomy, Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran. Correspondence should be addressed M. Jahanshahi (e-mail: mejahanshahi@yahoo.com). INTRODUCTION Alzheimer’s disease (AD) is manifested as a progressive cognitive and memory dysfunction syndrome, accompanied by neuropathological features, in particular extracellular deposition of amyloid-β (Aβ) proteins and intraneuronal accumulation of neurofibrillary tangles [1]. Aβ-induced neurotoxicity and oxidative stress are major contributors to the pathogenesis of AD [2]. In various brain regions, especially in the hippocampus, i.e., a structure significantly involved in cognition and memory, Aβ peptide accumulation contributes to progressive neuronal death [3]. In AD patients, anti-aggregation and anti-Aβ deposition treatments reduce Aβ deposition in the brain and alleviate cognitive disabilities. However, although this is a major goal in AD treatment, only a few drugs can induce some clearance of Aβ deposits [4]. High concentrations of 2-aminoethanesulfonic acid (taurine) are typical of the mammalian brain. Taurine is involved in a variety of biological processes, including the development of the retina and CNS in general, neuromodulation, calcium homeostasis, osmoregulation, antioxidant functions, membrane stabilization, and neuroprotection [3, 5]. It also performs a range of physiological functions in the liver, heart, kidney, retina, pancreas, and brain, and its depletion can increase the risk of several diseases (e.g., Parkinson’s disease, diabetes, cardiovascular diseases, AD, and neuronal damage in the retina) [6]. In a previous study, taurine was found to attenuate Aβ1-42-induced cognitive disorders, as well as neuronal damage, in a transgenic mouse AD model, owing to its neuroprotective and antioxidant properties [7]. Nonetheless, the potential therapeutic and protective effects of taurine against scopolamine-induced Aβ accumulation remained to be clarified. DOI 10.1007/s11062-019-09810-y