ارتباط تغییرات سطح سرمی پروتیین S100β و بیان ژن سلادین-یک هیپوکامپ در مدل آلزایمر اسپورادیک حیوانی

Background: Seladin-1 protein protects the neural cells against amyloid beta toxicity and its expression decreased in vulnerable regions of Alzheimer's disease (AD) brains. On the other hand, changes in serum levels of S100 have been considered as a marker of brain damage in neurodegenerative diseases. Furthermore, this study was carried out to determine the relation between the change profile of serum S100&beta protein levels and hippocampal Seladin-1 gene expression in a rat model of sporadic AD. Methods: In this experimental study that established in Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Science, from March 2011 to April 2013, 72 animals were randomly divided into control, 4, 7, 14, and 21days ICV-STZ/Saline administrated rats. Alzheimer's model was induced by intracerebroventricular (ICV) injections of streptozotocin (STZ) [3 mg/kg] on days 1 and 3. Serum levels of S100&beta and hippocampal Seladin-1 gene expression were evalu-ated in experimental groups. The initial and step-through latencies (STL) were deter-mined using passive avoidance test. Results: Serum levels of S100&beta were significantly different between the STZ-7 day and STZ-14 day groups in comparison with the control, saline and STZ-4 day groups. As well as, there was a significant difference between the STZ-7 day group in comparison with the STZ-14 day and STZ-21 day groups (P=0.0001). Hippocampal Seladin-1 gene expression in STZ-14 day and STZ-21 day groups significantly decreased as compared to the control, saline and STZ-4 day groups (P=0.0001). However, significant correla-tion was detected between serum S100&beta protein decrement and Seladin-1 down regula-tion (P=0.001). Also, the STL was significantly decreased in 21 days ICV-STZ adminis-trated rats as compared to the control or saline groups (P=0.001). Conclusion: Monitoring the changes of serum S100&beta protein levels by relationship with changes in hippocampal Seladin-1 gene expression can be a useful indicator of neu-ronal damage in patients with Alzheimer's disease.