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۱Effect of Magnetic Tacrine–Loaded Chitosan Nanoparticles on Spatial Learning, Memory, Amyloid Precursor Protein and Seladin–1 Expression in the Hippocampus Of Streptozotocin–Exposed Rats
اطلاعات انتشار: International Clinical Neuroscience Journal، سوم،شماره۱، ۲۰۱۶، سال
تعداد صفحات: ۷
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by memory and cognitive dysfunction due to neuronal cell loss in higher brain centers. Senile plaques containing amyloid β (Aβ) are associated with this disease as well as a reduction in cholinergic neuron numbers. Tacrine is a reversible cholinesterase inhibitor in clinical use to treat moderate forms of AD. Chitosan nanoparticles represent an effective systemic delivery system for drugs. The application of tacrine–loaded chitosan nanoparticles has been shown to selectively increase tacrine concentrations in the brain tissue. In this study, we compared magnetic and non–magnetic tacrine–loaded chitosan nanoparticles for their bioactivity and neuroprotective potency in streptozotocin (stz)–induced neurodegeneration, an accepted animal model for AD. Male rats received a single injection of stz via an implanted cannula into the lateral brain ventricle. Tacrine (tac)–loaded chitosan nanoparticles were delivered into the tail vein. Spatial learning and memory were analyzed using the Morris water maze task. Amyloid precursor protein gene (APP) and seladin–1 gene expression were studied in the hippocampus by real time–PCR. Tac–loaded non–magnetic and tac–loaded magnetic chitosan nanoparticles improved spatial learning and memory after stz treatment with magnetic nanoparticles being most effective. Similarly, tac–loaded chitosan nanoparticles increased seladin–1 and reduced APP gene expression. Again, magnetic nanoparticles were more effective. These data reveal that tac–loaded non magnetic and tac–loaded magnetic chitosan nanoparticles to a higher extent improve brain deficits related to stz application. We conclude that the magnetic target drug delivery system is a promising therapeutic strategy to protect AD–related degenerating in the CNS.
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