@article{ author = {Ahmadi, Shamseddin and MohammadianFarsani, Arezoo and Karami, Zanyar and Khosrobakhsh, Farnoosh and Rostamzadeh, Jalal}, title = {Increase in Nociception Threshold and Decrease in Mu-Opioid Receptor Gene Expression in Liver of a Rat Model of Hepatic Encephalopathy}, abstract ={Introduction: Hepatic encephalopathy (HE) is a brain disorder with impairment of cognitive and motor functions caused by liver failure. The aim of this study was to evaluate changes in nociception threshold as well as gene expression of mu-opioid receptor 1 (MOR1) in rat liver after induction of HE. Materials and Methods: The male rats (280-320 g) were randomly divided into three groups of control (non-operated), sham (operated without common bile duct ligation) and a group with a common bile duct ligation (BDL) as an experimental model of HE. Changes in nociception threshold were assessed on day 21 of BDL, using a hotplate test. On day 21 of BDL, rats were weighed, sacrificed and total liver tissue was dissected and weighed, then percentage of liver to body weight was measured. In addition, blood samples were collected for biochemical analysis of serum, and a piece of the liver of each rat was dissected for evaluating the MOR1 gene expression. Results: The results showed that nociception threshold, percentage of liver to body weights, and serum levels of total bilirubin were significantly increased in the HE model group compared to the sham group (P<0.001). Blood urea nitrogen was also increased in this group compared to the sham group (P<0.01). The results also revealed that the MOR1 gene expression at mRNA levels in liver of rats with BDL was significantly decreased compared to the sham group (P<0.001). Conclusion: Our data indicate that chronic liver failure modulates the MOR1 gene expression in liver. In addition, changes in nociception threshold may confirm a slowness of sensory processing in HE.}, Keywords = {Liver Failure, Brain Diseases, Bilirubin, Urea}, volume = {3}, Number = {1}, pages = {1-10}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.1}, url = {http://shefayekhatam.ir/article-1-643-en.html}, eprint = {http://shefayekhatam.ir/article-1-643-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Amiri, Sepideh and Eidi, Akram and Gorji, Ali}, title = {The Effect of Repetitive Cortical Spreading Depression on the Expression of GABA Aα Receptors in the Mesencephalic Trigeminal Nucleus in Male Adult Rats}, abstract ={Introduction: Spreading depression (SD) is a pathophysiologic phenomenon followed by a transient reduction in neuronal activity. Several studies indicate that SD plays a role in some neurological disorders. The present study is aimed to investigate the effect of SD on the expression of GABA A&alpha; receptors in the mesencephalic trigeminal nucleus. Materials and Methods: Animals were randomly classified into three control, sham, and experimental groups. Animals were anesthetized and during the stereotaxic surgery, recording electrodes and the injection cannula were implanted over the cortex. In the experimental group, KCl solution was injected four times once a week into the neocortex to induce repetitive SD. In sham group Ringer solution was injected and control group received no intervention. At the end of this stage, the animals were perfused and the brains were removed. Consequently, histological examination of the brains and immunohistochemical staining method were used to investigate the mean number of dark neurons as well as the expression of GABA A&alpha; receptors and GAD65 enzyme. Results: The mean number of dark neurons significantly increased in the experimental group compared to the sham and control groups. Expression of GABA A&alpha; receptors and GAD65 enzyme in mesencephalic trigeminal region decreased significantly after SD in the experimental group compared to the other groups. Conclusion: Our findings indicate that SD modulates inhibitory receptors in mesencephalic trigeminal region. This may be important in treatment of cephalalgia.}, Keywords = {Cortical Spreading Depression, gamma-Aminobutyric Acid, Neocortex}, volume = {3}, Number = {1}, pages = {11-20}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.11}, url = {http://shefayekhatam.ir/article-1-650-en.html}, eprint = {http://shefayekhatam.ir/article-1-650-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {JalaliKondori, Bahman and Asadi, Mohammad Hossein and Azemati, Fateme}, title = {Subcloning of NGF Gene into pSecTag2/Hygro Secretory Vector and Expression in PC12 Cell Line}, abstract ={Introduction: Subcloning of specific genes in plasmids and transfecting them into target cells for producing therapeutic proteins or cell differentiation, is suggested as one of the most effective treatment methods for different diseases. Nerve growth factor (NGF) is one of the members of the neurotrophin family. Neurotrophins are a family of proteins that regulate the survival, differentiation, and function of different types of neurons. Studies showed that NGF gene expression in stem cells induces differentiation toward neuron-like cells as well as the growth of axons and its branching. Materials and Methods: In this research, enzymatic digestion on a plasmid carrying NGF gene was performed and extracted. NGF gene was subcloned into pSecTag2/Hygro secretory plasmid. The subcloned plasmid was precipitated and concentrated. It was then transfected by Lipofectamine into PC12 cell line. NGF gene expression and protein production were evaluated using RT-PCR and western blot methods. Results: Sequence determination indicated that secretory plasmid subcloning process has been correct. Expression of NGF gene in transfected PC12 cells was shown by RT-PCR method and production of its protein was proved by the results from western blots. Conclusion: Subcloning of NGF gene in pSecTag2 secretory vector is a suitable technique for transfer to eukaryotic cells.}, Keywords = {Transfection, Genetic Vectors, Nerve Growth Factors, PC12 Cells }, volume = {3}, Number = {1}, pages = {21-28}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.21}, url = {http://shefayekhatam.ir/article-1-645-en.html}, eprint = {http://shefayekhatam.ir/article-1-645-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Divanbeigi, Arash and Rohani, Younos and Divanbeigi, Ashk}, title = {Investigating the Neurological Signs and Symptoms of Patients before Anterior Cervical Discectomy}, abstract ={Introduction: Degenerative disc disease is induced by the collapse of the anatomical structures of the spine. When symptoms are unbearable or does not respond to non-surgical treatments or there is a strong probability to damage to the spinal cord, discectomy is the suggested treatment. The purpose of this study was to explain the patient’s signs and the severity of neurological symptoms prior to surgery. Materials and Methods: This is a retrospective study with review of the clinical records of 103 patients were candidates for anterior cervical discectomy. Data were collected and analyzed by descriptive statistical tests. Results: The mean age of patients was 50.28±13.01 with the range of 25 to 71 years. The mean time from onset of symptoms to hospitalization for surgery was 2.70±1.94 months. Forty-one patients were smokers. In all cases, the first symptom was neck pain. There was radiculopathy in 55 cases (53.39%), radiculomyelopathy in 44 cases (42.71%), and myelopathy in 4 patients (3.88%). Forty-seven patients (45.63%) had disc degeneration at one level, 53 patients (51.45%) at two levels and 3 patients (2.91%) at three levels. Conclusion: The clinical status of patients before discectomy is the most important indicator for immediate patient referral to the surgeon.}, Keywords = {Diskectomy, Intervertebral Disc Degeneration, Neurologic Manifestations}, volume = {3}, Number = {1}, pages = {29-35}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.29}, url = {http://shefayekhatam.ir/article-1-652-en.html}, eprint = {http://shefayekhatam.ir/article-1-652-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Lotfinia, Ahmad Ali and Jafarian, Maryam and ModarresMousavi1, Mostafa and HosseiniRavandi, Hassan and Karimzadeh, Farib}, title = {Role of Laterodorsal Thalamic Nucleus during Absence Seizure Attacks}, abstract ={Introduction: A typical absence epilepsy is a type of nonconvulsive and generalized epilepsy. The main feature of these attacks is a sudden brief impairment of consciousness. The disturbances in thalamocortical loop play an important role in pathogenesis of absence seizures. However, it is not clear that which part of this network triggers the seizure. This study was aimed to investigate the role of latrodorsal (LD) thalamic neurons during spike and wave discharges (SWDs) in WAG/Rij rats, as the most valid animal model of absence epilepsy. Materials and Methods: Single unit activities in the LD thalamic nucleus and electrocorticogram of somatosensory cortex were simultaneously recorded in six-month-old WAG/Rij rats. Results: During SWDs, unit activity in the LD thalamic nucleus showed burst-like discharges, which were started before the peak component of SWDs. In SWD-free periods, burst like activity in the LD was reduced. Conclusion: Our findings suggest that the burst firing of LD may stimulate the neocortex to exhibit SWDs. It can be concluded that inhibition of burst firing of LD neurons may reduce the frequency of SWDs.}, Keywords = {Epilepsy, Absence, Thalamus, Rats, Somatosensory Cortex}, volume = {3}, Number = {1}, pages = {36-41}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.36}, url = {http://shefayekhatam.ir/article-1-653-en.html}, eprint = {http://shefayekhatam.ir/article-1-653-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {ZamaniEsmati, Mahya and Malakzadeh, Hanieh and JenabEsfahani, Hanieh and Eshaghabadi, Arezou and Ghasemi, Sedigheh and Jafarian, Maryam}, title = {The Effect of Carbamazepine on Neuronal Damage in Pentylentetrazole Model of Seizure}, abstract ={Introduction: Epilepsy is the most common disorder of the central nerves system. Studies showed that carbamazepine has anti-epileptic effects. However, there is no evidence whether carbamazepine protect seizure-induced neuronal injury. In this study, the effects of carbamazepine were evaluated on cell injury observed in pentylenetetrazole (PTZ) model of seizure in the rat brain. Materials and Methods: The convulsive behaviour and histological evaluation were performed in age- and weight-matched rats, which were divided into five groups: 1.control group: without any intervention, 2. PTZ group: after PTZ injection (40 mg/ kg), 3. Sham group: vehicles were injected 30 min before PTZ injection (40 mg/ kg), 4. Treatment group 1: carbamazepine (10 mg/kg) was injected 30 min before PTZ injection, 5. Treatment group 2: carbamazepine (40 mg/kg) was injected 30 min before PTZ injection. Results: Carbamazepine significantly decreased production of the dark neurons in the hippocampal CA1 and CA3 areas and the temporal cortex after PTZ-induced seizure compared to PTZ and sham groups. Density of dark neurons in treatment groups was significantly higher than control group. Conclusion: The results showed that carbamazepine acts as a neuroprotective substance after seizure attacks.}, Keywords = {Carbamazepine, Epilepsy, Seizures, Pentylenetetrazole, Hippocampus}, volume = {3}, Number = {1}, pages = {42-48}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.42}, url = {http://shefayekhatam.ir/article-1-654-en.html}, eprint = {http://shefayekhatam.ir/article-1-654-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {SahabNegah, Sajad and MohammadSadeghi, Shahin and Kazemi, Hadi and ModarresMousavi, Mostafa and Aligholi, Hadi}, title = {Effect of Injured Brain Extract on Proliferation of Neural Stem Cells Cultured in 3-Dimensional Environment}, abstract ={Introduction: After primary brain injury, secondary mechanisms are activated and lead to releasing of various supportive and neurotrophic factors in injured tissues. The effect of the new environment on neurogenesis, proliferation, and survival of stem cells needs more investigations. The aim of the present study was to evaluate the effect of injured brain extract on proliferation of embryonic rat neural stem cells (NSCs). Materials and Methods: NSCs were isolated from ganglionic eminences of embryonic rat then cultured as neurospheres. Next, cells were seeded in PuraMatrix scaffold as 3-dimension culture. Based on the medium content, cells were divided into 4 groups: with growth factor, without growth factor, without growth factor + intact brain extract, and without growth factor + injured brain extract. Proliferation assay was done by evaluation of the DiI labeled cells and the survival assay was carried out by MTS test 10 days later. For preparation of the injured brain extract, a rat brain injury model was utilized and the extract was collected 48 hours after brain injury. Results: The results showed that NSCs derived ganglionic eminence of embryonic rat had high proliferation ability. DiI-positive cells and MTS test showed a higher tendency of the proliferation and survival of NSCs in the without growth factor + injured brain extract and growth factor groups compared to the without growth factor and without growth factor + intact brain extract groups. Conclusion: Our results indicated a possible positive impact of injured brain extract on survival and proliferation of rat embryonic neural stem cells. Further studies are needed to investigate our preliminary findings in details.}, Keywords = {Neural Stem Cells, Brain Injuries, Tissue Extracts, RADA16-I }, volume = {3}, Number = {1}, pages = {49-56}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.49}, url = {http://shefayekhatam.ir/article-1-646-en.html}, eprint = {http://shefayekhatam.ir/article-1-646-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Ahmadi, Milad and Karimi-Godarzi, Ali and Alizadeh, Leil}, title = {The Role of AMPA Receptor in the Basolatral Amygdala on Aggression and Anxiety in Rats}, abstract ={Introduction: According to the previous studies, neural pathway of the basolatral amygdala plays an important role in etiology and pathophysiology of depression, anxiety, and aggression. However, the exact role of the basolateral amygdala in anxiety needs to be elucidated. Using social interaction and elevated plus maze tests, the role of AMPA glutamate subreceptors in the basolatral amygdala on aggression and anxiety-like behaviors was investigated. Materials and Methods: After anesthesia, two cannulas were implanted in the basolatral amygdala in Wistar rats. After one week recovery, anxiety levels and different forms of aggression were analyzed by elevated plus maze and social interaction tests. Results: AMPA agonist was administered at 0.25, 0.5, and 1 mg/kg doses in the basolateral amygdala. Doses of 0.5 and 1 mg/kg were significantly increased time spent in the open arms and offensive sideway compared to sham group. In addition, activation of AMPA receptor at 1 mg/kg significantly decreased the stay and entrance percentage of open arm and offensive sideway. Conclusion: Our data indicate that AMPA receptors modulate the signaling in the basolateral amygdala and may affect anxiety and aggression.}, Keywords = {Receptors, AMPA, Amygdala, Anxiety, Aggression}, volume = {3}, Number = {1}, pages = {57-64}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.57}, url = {http://shefayekhatam.ir/article-1-655-en.html}, eprint = {http://shefayekhatam.ir/article-1-655-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {EsteghamatHanzai, Samaneh and MoghadamiMonaghi, Sanaz and Gorji, Ali}, title = {Prevalence of Overweight and Obesity in Patients with Spinal Cord Injury}, abstract ={Introduction: Obesity is one of the most prevalent diet-related problems and increases the risk for diabetes mellitus, hypertension, atherosclerosis, and dyslipidemia. Cardiovascular diseases are one of the major of morbidity and mortality in people with a spinal cord injury (SCI). Increased fat mass has also been identified as an important risk factor in chronic SCI and weight management is recommended as an important preventive strategy of cardiovascular disease. The aim of this study is to determine the prevalence of overweight and obesity in people with SCI. Materials and Methods: An observational analytic cross sectional study was done on 850 SCI patients registered in Khatam Alanbia Hospital, Tehran, Iran, from 2008 to 2013. These data are included age, sex, height, weight, duration of SCI, and the level of SCI. The body mass index (BMI) was subsequently calculated for each patient and the prevalence of overweight and obesity were determined. Results: Of the 850 patients, 833 patients were male and 17 were female. In all, 50.2% of patients had a normal BMI and 7.6% of patients were undernourished. The prevalence of overweight and obesity were 32.1% and 10%, respectively. There was a significant relation between age and body mass index but there was no significant correlation between the level of injury and body mass index. Conclusion: Prevalence of overweight and obesity are high in people with SCI and there is a significant positive correlation between BMI and age.}, Keywords = {Spinal Cord Injuries, Obesity, Body Mass Index}, volume = {3}, Number = {1}, pages = {65-70}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.65}, url = {http://shefayekhatam.ir/article-1-656-en.html}, eprint = {http://shefayekhatam.ir/article-1-656-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {SahabNegah, Sajad and Khaksar, Zabihollah and MohammadSadeghi, Shahin and Erfanimajd, Naeem and ModarresMousavi, Mostafa and Aligholi, Hadi and Adibmoradi, Masoud and Moradi, Hamid Rez}, title = {Effect of Nettle Root Extract on Histometrical Parameters of Cerebral and Cerebellar Cortices in Rat Following Administration of Testosterone}, abstract ={Introduction: Testosterone is a steroid hormone secreted by gonads and adrenal glands. High dose of testosterone leads to decrease neurogenesis and induce apoptosis in vitro. To modulate testosterone effect, plants contain anti-androgenic properties can be useful. Urtica dioica, often called common nettle, contains anti-androgen compounds. Furthermore, the phytoestrogens effects of nettle have been evaluated. In this study, the effect of nettle root extract on histological structures of the cerebral and cerebellar cortices of rats was evaluated after testosterone injection. Materials and Methods: Twenty healthy adult male Wistar rats were divided randomly into 4 groups: control group (received ordinary feed without any treatment), testosterone group (received 10 mg/kg testosterone subcutaneously), nettle root extract group (received 50 mg/kg nettle root extract orally), nettle + testosterone group (received 50 mg/kg orally nettle root extract and 10 mg/kg testosterone). After 6 weeks, the brains were stained by hematoxylin and eosin. The number of neuronal cell body, nuclear diameter of neurons, diameter of Purkinje cells, and diameter of cerebellar layers were measured. Results: There were no significant differences in the mean number of neuronal cell body in cerebral cortex, diameter of Purkinje cells in cerebellum, and thickness of cerebellar layers among different groups. The nuclear diameter of neurons in inner granular layer of cerebrum in the testosterone group significantly increased compared to the nettle and nettle + testosterone groups. Conclusion: Nettle plant can be considered as a testosterone modulator. To determine more precise effect of nettle on the brain, further studies are needed.}, Keywords = {Brain, Rats, Urtica dioica, Testosterone}, volume = {3}, Number = {1}, pages = {71-78}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.71}, url = {http://shefayekhatam.ir/article-1-659-en.html}, eprint = {http://shefayekhatam.ir/article-1-659-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Faridaalaee, Gholamreza and Pashapour, Ali and KeigobadiKhajeh, Fatemeh}, title = {Subdural Hematoma Mimics Epidural Hematoma: A Case Report}, abstract ={Introduction: Traumatic brain injuries (TBI) are complex injuries with a broad range of symptoms and disabilities. TBI include epidural hematoma (EDH), subdural hematoma (SDH), intracerebral hemorrhage, subarachnoid hemorrhage (SAH), diffuse axonal injury, and brain contusion. Case Description: The patient was a 22-year-old man referred to the emergency department of Imam Khomeini hospital, Urmia, Iran, suffering from headache. Headache severity was 8 out of 10 (according to visual analog scale). The patient was fully alert and Glasgow coma scale was 15. Brain CT scan showed EDH and blood that filled the sylvain fissure. Results: It was revealed during surgery that patient was suffering from SDH with bleeding in a chronic arachnoid cyst. Conclusion: SDH is the collection of blood in the space between the dura and subarachnoid layer and originating from veins. SDH is more common in alcoholic and older patients. In rare cases, blood is collected arachnoid cyst and is seen like SAH.}, Keywords = {Hematoma, Subdural, Hematoma, Epidural, Cranial, Brain, Subarachnoid Hemorrhage}, volume = {3}, Number = {1}, pages = {79-83}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.79}, url = {http://shefayekhatam.ir/article-1-644-en.html}, eprint = {http://shefayekhatam.ir/article-1-644-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Ghayour, Mohammad Bagher and Abdolmaleki, Arash and Fereidoni, Masou}, title = {Use of Stem Cells in the Regeneration of Peripheral Nerve Injuries: an Overview}, abstract ={Introduction: Peripheral nervous system has an innate regenerative ability that many factors are involved in its formation, such as Schwann cells, growth factors, and extracellular matrix. However, in severe injuries, peripheral nerve regeneration process is very weak and ineffective and therapeutic measures are needed for nerve regeneration. Current therapeutic methods have several limitations and low efficacy. In this regard, one of the most important research approaches is using stem cells in the regeneration of peripheral nerves. Stem cells have a potential to differentiate into Schwann cells. Stem cells modulate the immune system by secreting neurotrophic factors and help formation of myelin layer during peripheral nerve regeneration. Researches in this field also represent these capabilities and promise a bright future in the application of stem cells in the regeneration of peripheral nerve injuries. Conclusion: Regarding the importance of stem cells in the future of regenerative medicine and neurological tissue engineering, understanding of characteristics of stem cells as well as recognition of the extraction resource and their abilities in promoting the peripheral nerve regeneration are necessary. This paper is a review of the most important progress that has been achieved in this field.}, Keywords = {Peripheral Nerves, Regeneration, Schwann Cells, Stem Cells}, volume = {3}, Number = {1}, pages = {84-98}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.84}, url = {http://shefayekhatam.ir/article-1-660-en.html}, eprint = {http://shefayekhatam.ir/article-1-660-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Seghatoleslam, Masoumeh and Hosseini, Mahmou}, title = {Potential of Stem Cells in the Treatment of Nervous System Disorders}, abstract ={Introduction: The stem cells are undifferentiated cells that have a potential to produce many different cell types in the body. A vast amount of data indicates the potential of stem cell therapy for various neurological diseases. In the present review, the possible beneficial effects of stem cells for treatment of nervous system disorders were presented. The stem cells have been suggested for treatment of different acute and chronic nervous system disorders such as hemorrhagic as well as ischemic stroke, Parkinson's disease, Hantington's disease, amyotrophic lateral sclerosis, multiple sclerosis, and Alzheimer's disease. Conclusion: Stem cells have been frequently examined in experimental studies and may be considered as the new developing strategies to treat nervous system disorders in the near future.}, Keywords = {Stem Cells, Nervous System Diseases, Therapeutics}, volume = {3}, Number = {1}, pages = {99-114}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.99}, url = {http://shefayekhatam.ir/article-1-642-en.html}, eprint = {http://shefayekhatam.ir/article-1-642-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Samadi, Ali}, title = {Exercise Preconditioning and Neuroprotection: A Review of Mechanisms}, abstract ={Introduction: Cerebrovascular accident or stroke is the first cause of acquired disability and the third leading cause of mortality in adults. It is known that exercise modifies risk factors such as hypertension, lipid profile, diabetes that may play an important role in the prevention of cerebrovascular accidents. However, recent findings suggest that besides adjusting the risk factors of stroke, exercise may be helpful in inducing endogenous neuroprotection and neuronal survival in ischemia – reperfusion condition which is the main mechanism of ischemic stroke. The effect of previous exercises in protecting neurons against ischemic injury and inducing neuronal resistance known as exercise preconditioning, which is a relatively new field of research on the effects of exercise on the brain. Although the exact mechanisms of neuroprotection induced by exercise preconditioning have yet to be known, previous studies have shown that exercise preconditioning may be helpful through several mechanisms, such as strengthening blood-brain barrier, inducing cerebral angiogenesis and arteriogenesis, improving cerebral metabolism and decreasing neuronal metabolic disturbances following ischemic injury, upregulation of neurotrophins expression, as well as reducing inflammation, apoptosis, and oxidative stress. Conclusion: It seems that exercise preconditioning in people predisposed to brain ischemic injuries or in people with history of mild ischemic injury may help in reducing the primary damage and improve the neurological outcomes after ischemia-reperfusion injury. However, more research is needed to develop exercise protocols with appropriate time, intensity, and type to induce the optimal neuroprotection.}, Keywords = {Exercise, Stroke, Ischemia}, volume = {3}, Number = {1}, pages = {115-130}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.115}, url = {http://shefayekhatam.ir/article-1-648-en.html}, eprint = {http://shefayekhatam.ir/article-1-648-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Parvini, Neda and Ahmadi, Shamseddi}, title = {Role of MicroRNAs in Development of Immune Cells and Nervous System and their Relation to Multiple Sclerosis}, abstract ={Introduction: MicroRNAs (miRNAs) are small and non-coding ribonucleic acids that play critical roles in regulation of host genome expression at post-transcriptional level. An individual miRNA is able to down-regulate multiple targeted mRNA transcripts. Therefore, minor changes in a miRNA expression may lead to significant alterations in the expression of different genes. During last two decades, miRNAs have emerged as key regulators of immune cell lineage differentiation, maturation, maintenance of immune homeostasis, and normal function. Multiples sclerosis (MS) is a chronic inflammatory disease that is characterized by infiltration of lymphocytes into the central nervous system (CNS), demyelination and axonal degeneration. Although causes of MS are still unknown, it is widely accepted that novel drug targets need to focus on both decreasing inflammation and promoting CNS repair. Recent researches about MS disease have shown that miRNAs are dysregulated in the immune system and CNS, which shows their role in the MS pathogenesis. Conclusion: Identification of specific expression patterns of miRNA in autoimmune diseases and a further comprehensive understanding of their role in the pathogenesis of different diseases offers promise of not only novel molecular diagnostic markers but also new gene therapy strategies for treating inflammatory autoimmune diseases. In this study, we review the latest findings about miRNA biogenesis and signatures in the CNS and immune cells of MS patients.}, Keywords = {MicroRNAs, Inflammation, Autoimmunity, Central Nervous System, Demyelinating Diseases}, volume = {3}, Number = {1}, pages = {131-144}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.131}, url = {http://shefayekhatam.ir/article-1-647-en.html}, eprint = {http://shefayekhatam.ir/article-1-647-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {BabaeiAbraki, Shahnaz and Chavoshi-Nezhad, Sar}, title = {Alzheimer’s Disease: The Effect of Nrf2 Signaling Pathway on Cell Death Caused by Oxidative Stress}, abstract ={Introduction: There is an increasing prevalence of Alzheimer's disease (AD). Amyloid-beta deposition and neurotoxicity play an effective role in AD. Oxidative stress is thought to be central in the pathogenesis that leads to production of reactive oxygen species and causing damages of the macromolecules in target cells. It has been reported that the nuclear factor erythroid 2 related factor 2 (Nrf2) is a key regulator of endogenous inducible defense systems in the body and increase the level of many antioxidants, including glutathione-s-transferase. Under oxidative damage conditions, Nrf2 translocates to the nucleus, binds to the antioxidant response element (ARE), and enhances sequence to initiate transcription of cytoprotective genes. This review focuses on cellular mechanisms of Nrf2 regulation and discusses the relationship between Nrf2 regulation and AD. Conclusion: In general, we suggest that Nrf2-ARE activation is a novel neuroprotective pathway that can be consider as a promising therapeutic strategy for the treatment of neurodegenerative disorders, such as AD.}, Keywords = {Alzheimer Disease, Amyloid beta-Peptides, Oxidative Stress, Reactive Oxygen Species}, volume = {3}, Number = {1}, pages = {145-156}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.145}, url = {http://shefayekhatam.ir/article-1-661-en.html}, eprint = {http://shefayekhatam.ir/article-1-661-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} } @article{ author = {Divanbeigi, Ashkan and Divanbeigi, Arash}, title = {A Brief Review on the Causes of Autism Spectrum Disorder}, abstract ={Introduction: Nowadays, many researchers apply autism spectrum disorder (ASD) to describe pervasive developmental disorders. In this model, the differences of previous three common pervasive developmental disorders, including autism disorder, Asperger’s disorder, and pervasive developmental disorder not otherwise specified, point to the various levels and not the type of disorder. According to the importance and poor prognosis as well as the lack of awareness of this disorder among Iranian people, this article discusses the most important causes of ASD. Conclusion: There is no single cause has still been known for ASD. However, ASD may be caused by the interactions of neurobiological and environmental factors with genetic susceptibility.}, Keywords = {Child Development Disorders, Pervasive, Heredity, Neurobiology}, volume = {3}, Number = {1}, pages = {157-166}, publisher = {Shefa Neuroscience Research Center}, doi = {10.18869/acadpub.shefa.3.1.157}, url = {http://shefayekhatam.ir/article-1-662-en.html}, eprint = {http://shefayekhatam.ir/article-1-662-en.pdf}, journal = {The Neuroscience Journal of Shefaye Khatam}, issn = {2322-1887}, eissn = {2345-4814}, year = {2015} }