Basic and Clinical Neuroscience
Volume:7 Issue: 2, Spring 2016

Many studies indicate that oxidative stress is involved in the pathophysiology of neurodegenerative diseases. Oxidative stress can induce neuronal damages, modulate intracellular signaling and ultimately leads to neuronal death by apoptosis or necrosis. To review antioxidants preventive effects on oxidative stress and neurodegenerative diseases we accumulated data from international medical journals and academic information's sites. According to many studies, antioxidants could reduce toxic neuronal damages and many studies confirmed the efficacy of polyphenol antioxidants in fruits and vegetables to reduce neuronal death and to diminish oxidative stress. This systematic review showed the antioxidant activities of phytochemicals which play as natural neuroprotectives with low adverse effects against some neurodegenerative diseases as Parkinson or Alzheimer diseases.

Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS.
A review of literature for eligible genetic association Studies published before October 20, 2014 was conducted in the PubMed, EMBASE, Google Scholar and Trip database. The strength of association was calculated by pooled odds ratios (ORs) with 95% confidence intervals using RevMan 5.3 software. Heterogeneity was examined using Higgins I-squared, Tau-squared, and Chi-squared tests.
A total of 2 studies involving 614 cases and 617 controls were found. The overall estimates did not show any significant relation between TGF-β1-509C/T polymorphism and risk of IS under dominant (CC vs. TT: OR=1.01, 95%CI=0.31 to 3.26; P=0.99), recessive (CC vs. CT: OR=0.94, 95%CI=0.47 to 1.90; P=0.87), and allelic models (T vs. C: OR=1.06, 95%CI=0.55 to 2.04; P=0.86).
This meta-analysis showed that TGF-β1-509C/T gene polymorphism no significant association with the susceptibility of IS. Further well-designed prospective studies with larger sample size are needed to confirm these findings.

To study the effect of gallic acid (GA) on hippocampal long-term potentiation (LTP) and histological changes in animal model of Alzheimer disease (AD) induced by betaamyloid (Aβ).
Sixty-four adult male Wistar rats (300±20 g) were divided into 8 groups: 1) Control (Cont); 2) AD; 3) Sham; 4-7) AD (50, 100, and 200 mg/kg for 10 days, orally) or vehicle, 8) Cont᠍, Aβ (1μg/μL in each site) was infused into hippocampus bilaterally. Changes of amplitude and slope of LTP induced in hippocampal dentate gyrus (DG) were evaluated by high frequency stimulation (HFS) of perforant path (PP).
Data showed that LTP amplitude and area under curve significantly impaired in AD rats (P Current findings suggest that GA reduces neural damage and brain amyloid neuropathology and improves cognitive function via free radicals scavenging and inhibiting oligomerization of Aβ but with no effect on healthy rats.

Huntington disease (HD) is a progressive neurodegenerative disease which affects movement control system of the brain. HD symptoms lead to patient’s gait change and influence stride time intervals. In this study, we present a grey box mathematical model to simulate HDdisorders. This model contains main physiological findings about BG.
We used artificial neural networks (ANN) and predetermined data to model healthy state behavior, and then we trained patients with HD with this model. All blocks and relations between them were designed based on physiological findings.
According to the physiological findings, increasing or decreasing model connection weights are indicative of change in secretion of respective neurotransmitters. Our results show the simulating ability of the model in normal condition and diferent disease stages.
Fine similarity between the presented model and BG physiological structure with its high ability in simulating HD disorders, introduces this model as a powerful tool to analyze HD behavior.

Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS.
Male Wistar rats were divided into sham (receiving phosphate buffered saline within dorsal hippocampus), pilocarpine (epileptic model of TLE), single injection BDNF (epileptic rats which received single high dose of BDBF within dorsal hippocampus), and multiple injections BDNF (epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE) groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated.
Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group.
Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are necessary to clarify the exact mechanisms of BDNF effects.

Multiple sclerosis (MS) is generally known as a manageable but not yet curable autoimmune disease affecting central nervous system. A potential therapeutic approach should possess several properties: Prevent immune system from damaging the brain and spinal cord, promote differentiation of oligodendrocyte progenitor cells (OPCs) into mature oligodendrocytes to produce myelin, prevent the formation of fibronectin aggregates by astrocytes to inhibit scar formation, and enhance function of healthy endothelial cells (ECs).
To determine if an increase in sulfur contents through H2S, a potent antioxidant known to induce protective autophagy in cells, could provide the above desired outcomes, peripheral blood mononuclear cells (PBMNCs), OCPs, astrocytes, and ECs were treated with NaHS (50 μM) in vitro.
Transmigration assay using EC monolayer showed that serotonin increased migration of PBMNC while pretreatment of EC with NaHS inhibited the migration induced by serotonin treatment. NaHS upregulated proteins involved in immune system response and downregulated PBMNCs- and EC-related adhesion molecules (LFA-1 and VCAM-1). Furthermore, it had a cell expansion inducing effect, altering EC morphology. The effects of NaHS on OPCs and astrocytes were studied compared to mTOR inhibitor rapamycin. In NaHS treated astrocytes the induced fibronectin production was partially inhibited while rapamycin almost fully inhibited fibronectin production. NaHS slowed but did not inhibit the differentiation of OCPs or the production of myelin compared to rapamycin.
The in vitro results point to the potential therapeutic application of hydrogen sulfide releasing molecules or health-promoting sulfur compounds in MS.

Depression is a mental disorder that highly associated with immune system. Therefore, this study compares the serum concentrations of IL-21, IL-17, and transforming growth factor β (TGF-β) between patients with major depressive disorder and healthy controls.
Blood samples were collected from 41 patients with major depressive disorder and 40 healthy age-matched controls with no history of malignancies or autoimmune disorders. The subjects were interviewed face to face according to DSM-IV diagnostic criteria. Depression score was measured using completed Beck Depression Inventory in both groups. The serum concentrations of IL-21, IL-17, and TGF-β were assessed using ELISA.
The mean score of Beck Depression score in the patient and control groups was 35.4±5.5 and 11.1±2.3. IL-17 serum concentrations in the patients and the control group were 10.03±0.6 and 7.6±0.6 pg/mL, respectively (P=0.0002). TGF-β level in the patients group was significantly higher than compare to the control group; 336.7±20.19 vs. 174.8±27.20 pg/mL, (P0.05).
Considering pro-inflammatory cytokines, current results support the associationof inflammatory response and depressive disorder. So, it seems that pro-inflammatory factors profile can be used as indicator in following of depression progress and its treatment impacts.

Neurofeedback is a kind of biofeedback, which teaches self-control of brain functions to subjects by measuring brain waves and providing a feedback signal. Neurofeedback usually provides the audio and or video feedback. Positive or negative feedback is produced for desirable or undesirable brain activities, respectively. In this review, we provided clinical and technical information about the following issues: (1) Various neurofeedback treatment protocols i.e. alpha, beta, alpha/theta, delta, gamma, and theta; (2) Different EEG electrode placements i.e. standard recording channels in the frontal, temporal, central, and occipital lobes; (3) Electrode montages (unipolar, bipolar); (4) Types of neurofeedback i.e. frequency, power, slow cortical potential, functional magnetic resonance imaging, and so on; (5) Clinical applications of neurofeedback i.e. treatment of attention deficit hyperactivity disorder, anxiety, depression, epilepsy, insomnia, drug addiction, schizophrenia, learning disabilities, dyslexia and dyscalculia, autistic spectrum disorders and so on as well as other applications such as pain management, and the improvement of musical and athletic performance; and (6) Neurofeedback softwares. To date, many studies have been conducted on the neurofeedback therapy and its effectiveness on the treatment ofmany diseases. Neurofeedback, like other treatments, has its own pros and cons. Although it is a non-invasive procedure, its validity has been questioned in terms of conclusive scientific evidence. For example, it is expensive, time-consuming and its benefits are not long-lasting. Also, it might take months to show the desired improvements. Nevertheless, neurofeedback is known as a complementary and alternative treatment of many brain dysfunctions. However, current research does not support conclusive results about its efficacy.

Meningioma is a benign and slowly-growing tumor that is responsible for 20% of brain neoplasms. It can be accompanied by some genetic disorders such as neurofibromatosis type 2 and is more common among women. As a space occupying lesion, it produces a wide range of signs and symptoms by compressing the adjacent and underlying tissues in the brain. Trauma and viruses are possible etiologies for meningioma. The ideal treatment of benign meningioma is surgical resection.
In this case report, we present a middle-aged man with a seeding metastasis of the cranial meningioma (after its removal) in the left thigh. During the removal operation, fascia lata had been used to repair the dura mater and the skin defect was repaired primarily.
We believe that the occurrence of meningioma at the site of incision in the thigh is related to using the same surgical instruments for the removal of the brain tumor.

Hallervorden-Spatz syndrome is a disorder characterized by dystonia, parkinsonism, and iron accumulation in the brain. The disease is caused by mutations in gene encoding pantothenate kinase 2 (PANK2) and patients have pantothenate kinase-associated neurodegeneration. We present an 8-year-old boy with progressive muscle dystonia, neuroregression, frequent fall and multiple injury marks of different stages. Seizures are rare with PANK2. This child had seizure onset at 4 years of age and seizure free on valproate and levetricetam. The CT scan showed tiger eye appearance and mutations on PANK2 gene.

This study aimed to evaluate the effectiveness of neurofeedback on attention deficit hyperactivity disorder.
This is a quasi-experimental study without a control group. The study population included all children aged 5 to 12 years old affected with attention deficit hyperactivity disorders in Tehran, Iran who were referred to psychiatric clinics and given the diagnosis. The sample included 12 children with attention deficit hyperactivity disorder who were selected based on their availability (non-random sampling). They received 30 sessions of neurofeedback treatment, 2 times per week. Before and after neurofeedback training, the children were evaluated and compared with the use of cognitive assessment system test. Data were analyzed using dependent T-test.
The total mean score for pretest was 88.81 while the total mean score for the post test was 82.23. The mean in pretest for attention hyperactivity disorder was higher than the mean in the post test. Moreover, The difference of pretest and post test scores of children affected with learning disorder associated with ADHD was calculated that showed significant (P=0.003).
Neurofeedback is effective in the improvement of attention deficit hyperactivity disorder.