The effect of vitamin B12 on synaptic plasticity of hippocampus in Alzheimer’s disease model rats

Abstract

Background Hippocampus cells, responsible for learning and memory, are disturbed in Alzheimer’s disease (AD), resulting in production of several inflammatory markers, such as neurexin 1 –neuroligin, cyclooxygenase–2 (COX–2), and caspase–3 proteins, used in measurement of AD’s severity and development. Vitamin B12, which plays a role in brain functioning, has anti–inflammatory properties and its impairment is associated with apoptosis in Alzheimer’s disease. This study aimed to investigate the effect of vitamin B12 on restoration of Synaptic Plasticity on scopolamine–induced AD in rats. Methods To simulate AD, Rats, except the control group were i.p. injected with 3 mg/kg scopolamine. Before scopolamine the pretreatment group vitamin B12 (0.5, 2, and 4 mg/kg) was injected every day for the next 14 days. After 24 h, sectioning the rats’ brains, the concentration of postsynaptic density protein 95 (PSD–95), neurexin 1–neurolgin, COX–2, and caspase–3 proteins in hippocampus were measured using immunoblotting. Results B12 significantly enhanced molecular balance. PSD–95 and neurexin 1 and neuroligin concentrations were significantly reduced, whereas COX–2 and activated caspase–3 were enhanced in the hippocampus of scopolamine–injected subjects. Their alterations were decreased after B12 administration. Conclusions Vitamin B12 protected scopolamine–injected rats and inhibited hippocampal inflammation and apoptosis and preserved pre– and post–synaptic proteins and possibly synaptic integrity in hippocampus route.