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.
Full text
