Basic and Clinical Neuroscience
Volume:12 Issue: 4, Jul-Aug 2021

A major cause of injury and the second cause of death worldwide is stroke. Among several infectious agents considered as the risk factor of stroke, some pathogens demonstrated stronger robust associations with stroke. Proposing an accurate correlation between infectious microorganisms and stroke provides valuable information for early intervention and control of the infections. 

In this study, we searched the literature using the Web of Science, PMC/Medline via PubMed, and Scopus databases up to July 2018 without time and language restrictions. After quality assessment, 16 articles were included in the study. The whole data extraction process was independently conducted by two reviewers. 

Based on the results of the studies, viruses, such as Hepatitis C virus (HCV), Hepatitis B virus (HBV), Human Immunodeficiency Virus (HIV), Herpes Simplex Virus Type-1, 2 (HSV-1, 2), Varicella-Zoster Virus (VZV or Chickenpox), and West Nile virus (WNV) seem to be common causes of ischemic stroke. Moreover, the association of other microbial categories, such as Streptococcus mutans (in bacteria), Toxocara spp. and Toxoplasma gondii (in parasites), and Rhizopus sp. (in fungi) with stroke was reported. 

Considering the adverse role of the above-mentioned microorganisms, it is necessary to implement some preventive measures for stroke treatment.

Utilizing Functional Electrical Stimulation (FES) and rehabilitation robots for motion control is an open research problem. In this paper, a new control algorithm has been proposed which was de-signed based on a combination of FES and an active mechanical actuator to control the knee joint movement. 

An adaptive controller and a Proportional-Derivative (PD) controller have adjusted the mo-tor torque and stimulation intensity, respectively. The FES controller was activated whenever a dis-turbance observer detected the presence of the external disturbance. In this manner, the occurrence of the muscle fatigue arises from the FES can be postponed.

The simulation studies were carried out on a model of muscle-joint system along with a model of a servo-motor. The computed RMS of the tracking errors compared to the range of knee motion show that the tracking performance is acceptable. In this research, the trajectories envisioned as the knee joint reference trajectory were designed using the recorded human data.

The achieved results prove the ability of the proposed control strategy to not only reject the external disturbance but also compensate the muscle fatigue.

Parkinson’s Disease (PD) associates with changes in sex hormones; however, it remains unknown whether this is either a cause for or a result of the disease. To further evaluate it, we investigated if the development of 6-Hydroxydopamine (6-OHDA)-induced Parkinsonism changes the serum levels of testosterone and prolactin or not. 

6-OHDA was injected into the medial forebrain bundle using stereotaxic surgery. The development of Parkinsonism was evaluated by apomorphine-induced rotational test and the immunofluorescence labeling of Dopaminergic (DA) neurons in substantia nigra. The necessary blood samples were collected before the toxin and in the third and sixth weeks afterward. The hormones levels were determined using Enzyme-Linked Immunosorbent Assay (ELISA) kits.

The severity of rotations was different among 6-OHDA-treated rats; accordingly, they were divided into two subgroups of severe and mild parkinsonian rats. The degeneration of DA neurons was observed in both subgroups; however, it was significantly less in the mild group. In the sixth week after the toxin, testosterone level increased but only in the severe subgroup. Prolactin increased in both subgroups in the third week after the toxin but returned to normal in the sixth week. There was no association between the pre-toxin levels of these hormones and the intensity of Parkinsonism.

Our findings indicated that the development of 6-OHDA-induced Parkinsonism increases the serum levels of testosterone and prolactin. Increased prolactin occurred earlier and was observed in rats with less DA neuronal loss. Therefore, prolactin levels can predict the death of DA neurons before the clinical signs of PD were revealed.

Several computer-aided diagnosis systems for depression are suggested for use by clinicians to authorize the diagnosis. EEG may be used as an objective analysis tool for identifying depression in the initial stage to avoid it from reaching a severe and permanent state. However, artifact contamination reduces the accuracy in EEG signal processing systems.

This work proposes a novel denoising method based on Empirical Mode Decomposition (EMD) ( with Detrended Fluctuation Analysis (DFA) and wavelet packet transform. Initially, real EEG recordings corresponding to depression patients are decomposed into various mode functions by applying EMD. Then, DFA is used as the mode selection criteria. Further Wavelet Packets Decomposition (WPD)-based evaluation is applied to extract the cleaner signal. 

Simulations were conducted on real EEG databases for depression to demonstrate the effects of the proposed techniques. To conclude the efficacy of the proposed technique, SNR and MAE were identified. The obtained results indicated improved signal-to-noise ratio and lower values of MAE for the combined EMD-DFA-WPD technique. Additionally, Random Forest and SVM (Support Vector Machine)-based classification revealed the improved accuracy of 98.51% and 98.10% for the proposed denoising technique. Whereas the accuracy of the EMD- DFA is 98.01% and 95.81% and EMD combined with DWT technique equaled 98.0% and 97.21% for the EMD- DFA technique for RF and SVM, respectively, compared to the proposed method. Furthermore, the classification performance for both classifiers was compared with and without denoising to highlight the effects of the proposed technique.

Proposed denoising system results in better classification of depressed and healthy individuals resulting in a better diagnosing system. These results can be further analyzed using other approaches as a solution to the mode mixing problem of the EMD approach.

The Aphasia Check List (ACL) is a comprehensive, time-saving tool for language evaluation in aphasia, including a cognitive assessment part. This cross-sectional study aimed to translate ACL into Persian and analyze the psychometric features of the translated version. The original version of the ACL was translated and adapted from German; its psychometric features were then determined. 

Twenty People With Aphasia (PWA) and 50 age- and education-matched, cognitively healthy controls participated in this research. Possible floor and ceiling effects, discriminant validity, test-retest reliability, and internal consistency of the test were analyzed in addition to the evaluation of internal correlations between the test parts (language & cognition).

Regarding the performance of PWAs in the language section and the cognitive subtests assessing attention, memory, and reasoning, there were no floor and ceiling effects. Adequate discriminant validities for the language section of the test [i.e., total score: (Mann-Whitney U= 6.000, P<0.001); diagnostic subtests scores: (Mann-Whitney U= 3.000, P<0.001), and each subtest individually. Besides, the attention subtest of the cognition section (Mann-Whitney U= 16.500, P<0.001) was also observed. There was no difference between the control and patient groups in the subtests of memory (Mann-Whitney U= 497.500, P=0.973) and reasoning (Mann-Whitney U= 3.000, P= 308). The test-retest reliability was acceptable in all subtests (ICC agreement= 0.573-0.984). The ACL-P suggested appropriate internal consistency (Cronbach’s alpha coefficient= 0.761 for test & retest scores). There were also significant correlations between language and cognition in the control and patient groups.

The ACL-P test indicated sufficient reliability and validity for the evaluation of Persian-speaking PWAs and is suggested to be used in studies on this population.

Inflammatory processes in the brain play an important role in the etiopathogenesis of Obsessive-Compulsive Disorder (OCD). Cyclooxygenase inhibitors, such as celecoxib reduce the production of proinflammatory cytokines. This double-blind study aimed to investigate the effects of adding celecoxib to Selective Serotonin Reuptake Inhibitors (SSRIs)on treating OCD.

Sixty patients who met the diagnosis criteria for OCD based on the Diagnostic and Statistical Manual of Mental Disorders -Fourth Edition- Text Revision (DSM-IV-TR) were recruited in the present study. Two psychiatrists independently confirmed the diagnosis by performing structured interviews. The study participants included 23 patients who received SSRIs and celecoxib (400 mg twice daily) and 22 patients in the control group that received SSRIs and placebo. Moreover, at baseline, in weeks 4, 8, and 12, the explored patients were assessed by a psychiatrist using the Yale-Brown Obsessive-Compulsive Scale (Y-BCOS). 

A significant difference was observed in the change of scores on the Y-BOCS in week 12, compared with the onset of the study between the study groups (t= -8.976, df=38, P=0.001). There was a significant difference between the study groups in obsession (F= 49.19, df= 1, P≤0.001), compulsion (F= 13.78, df= 1, P= 0.001), and OCD (F= 57.25, df= 1, P≤0.001), i.e., higher in the celecoxib group. 

This study showed that adjuvant treatment with celecoxib can further improve the symptoms of OCD in individuals receiving SSRIs.

Depression and anxiety are the most common psychiatric disorders. These conditions widely occur in industrial societies and severely affect individuals’ lives. N-Acetylcysteine (NAC) is a mucolytic compound with antioxidant and anti-inflammatory effects. This study aimed to investigate the potential therapeutic effects of NAC on chronic noise-induced depression- and anxiety-like behaviors in mice.

Fifty male BALB/c mice were randomly divided into 5 groups, as follows: control, noise90 dB, noise110 dB, noise 90+NAC, and noise 110+NAC groups. Animals in the noise groups were exposed to 90 dB 2 h/day and 110 dB 2 h/day for 30 days. The NAC groups received NAC (325 mg/kg P.O.) 20 min after being exposed to noise. To evaluate depressive- and anxiety-like behaviors, the examined mice were subjected to the Open Field Test (OFT), Sucrose Preference Test (SPT), Tail Suspension Test (TST), and Elevated Plus Maze (EPM) tasks. At the end of the behavioral tests, the study animals were sacrificed. Accordingly, the levels of Malondialdehyde (MDA), Total Antioxidant Capacity (TAC), Superoxide Dismutase (SOD), and Glutathione Peroxidase (GPx) were determined in the Hippocampus (HIP) and the Prefrontal Cortex (PFC).

The obtained results suggested that noise exposure would induce anxiety- and depressive-like behaviors, being reversed by NAC administration. Moreover, chronic administration of NAC significantly increased antioxidant enzyme activities and reduced lipid peroxidation (MDA levels) in the PFC and HIP of noise-exposed mice.

Our findings revealed that administrating NAC would reduce the adverse effects of noise on the brain and would exert anti-depressant and anxiolytic effects.

Uteroplacental Insufficiency (UPI) produces critical neurodevelopmental problems affecting the Intrauterine Growth Restricted (IUGR) in offspring. This study aimed to investigate the possible neuroprotective roles of Hesperidin (Hes) on the fetal cerebral cortex of the UPI rat model.

In this experimental study, 40 pregnant Wistar rats (age: ~40 days, Mean±SD weight: 180±10 g) were randomly divided into 5 groups (n= 8/group). The study groups included control (normal saline, orally), UPI+NS (uterine vessel ligation+normal saline, orally), UPI+HES25, UPI+HES50, and UPI+HES100 (uterine vessel ligation+25, 50 and 100 mg/kg Hes, orally). After being anesthetized by ketamine and xylazine, UPI was induced by permanent bilateral closure of the uterine vessels on Gestation Day (GD) 18. From GD15, the Hes/NS-treated groups received Hes/normal saline until GD21. On GD21, the uterus, placenta, and fetus were dissected out and weighed. The oxidative stress parameters, including Catalase (CAT) activity, Malondialdehyde (MDA), and Total Antioxidant Capacity (TAC) were measured in the fetal cerebral cortex. The expression of Brain-Derived Neurotrophic Factor (BDNF) and Tropomyosin Receptor Kinase B (TrkB) was assessed by RT qPCR methods. The obtained data were analyzed by Analysis of Variance (ANOVA) and Tukey’s post hoc test.

The present study findings identified a significant difference in the uterine and fetus weight in Hes-treated mothers (P< 0.05). In the fetus, Hes reduced MDA, and increased CAT activity and TAC (P˂0.001 in the UPI+Hes100 group, compared to the UPI+NS group). UPI reduced BDNF and TrkB mRNA expression, compared to the control group (P<0.05). Also, Significant increases in BDNF and TrkB mRNA expression were observed after administrating Hes in the fetal cerebral cortex of the UPI rat model, in a dose-dependent manner (P<0.05).

Hes, as a neuroprotective and antioxidant agent, accelerates BDNF-TrkB signaling pathway and suppresses oxidative stress parameters in the cerebral cortex of the UPI rat model.

Retinal Pigment Epithelium (RPE) layer deterioration is a leading cause of Age-Related Macular Degeneration (AMD), i.e., the most significant reason for irreversible blindness. The present study aimed to track the Neurosphere-Derived (NS) from Bone Marrow Stromal Stem Cells (BMSCs) grafted into the sub-retinal space (destruction of the RPE layer by sodium iodate).

RPE degeneration model was performed using the injection of 5% sodium iodate performed in the retro-orbital sinus of Wistar rats. BMSCs were extracted from the examined rat femur and induced into NS, using EGF, bFGF, and B27. BrdU-NS labeled cells were transplanted into the sub-retinal space. For detecting BMSCs and NS markers, immunocytochemistry was performed. Moreover, immunohistochemical was conducted for tracking the transplanted cells in the RPE and sensory retina.

The immunocytochemistry of BMSCs cells displayed the expression of mesenchymal stem cells markers (CD90; 99%±1), CD166 (98%±2), CD44 (99%±1). Additionally, the expression of neural lineage markers in NS, such as SOX2, OCT4, Nanog, Nestin, and Neurofilaments (68, 160, 200) revealed the differentiation from BMSCs. Tracking BrdU-NS labeled suggested these aggregations in most layers of the retina.

Our study data indicated that BMSCs derived neurosphere had the potential to migrate in injured retinal and integrate into the neurosensory retina. These data can be useful in finding safe cells for replacement therapy in AMD.

Multiple Sclerosis (MS) is the chronic inflammation of the Central Nervous System (CNS) and autoimmune disease. MS is most widely considered to be mediated by the activation of myelin-specific T CD4+ cells as well as TH1 and TH17 cells. TH17 cells are involved in the pathogenesis of MS in various manners. HIF-1α and RORC are required for the natural differentiation of TH17; they are essential transcription factors for the evolution of TH17 cells. Numerous studies indicated that Epigallocatechin Gallate (EGCG) presents immunomodulatory and anti-inflammatory effects. This study investigated the effects of EGCG on normoxic HIF-1α and RORC2 expression in PBMCs among MS patients.

Peripheral Blood Mononuclear Cells (PBMCs) were isolated from the whole blood of new cases of MS. The cells were cultured in the presence of a different concentration of EGCG (25, 50,100μM) for 18 and 48 hours. Next, HIF-1α and RORC2 level expressions were measured by Enzyme-Linked Immunosorbent Assay (ELISA) and Real-Time PCR, respectively. 

The results showed that EGCG significantly decreased RORC2 gene expression. EGCG did not affect the level of HIF-1α. 

However, EGCG did not influence the level of HIF-1α. Our present data has led us to conclude that EGCG could be considered as an anti-inflammatory agent may serve as an achievable therapeutic agent for MS.

The current pilot study aimed to examine the short-term effects of ankle Elastic Therapeutic Taping (ETT) on static and dynamic balance. 

Twenty-Four individuals with chronic stroke were assigned to an experimental or control group (n=12/group); they both received Conventional Physical Therapy (CT) for 3 weeks, 3 times per week. The experimental group additionally underwent taping to the ankle of the paretic side continuously for 3 weeks. Standardized measures for static and dynamic balance were administered at pre-test and post-test and analyzed using Wilcoxon and Analysis of Covariance (ANCOVA).

The experimental group significantly improved on two measures, Biodex anterior-posterior static (P=0.03) and medial-lateral dynamic (P=0.04) balance indices, compared to the controls. Both groups improved within their respective groups for Berg Balance Scale and Functional Reach (P<0.05). Static balance consistently improved across measures with the experimental intervention with large effect sizes.

Ankle ETT, combined with CT, may be effective in the short-term for improving static and dynamic balance in stroke, compared to CT alone. A future larger randomized trial with longer follow-up is required to establish this method’s effectiveness.

Cognitive Remediation Therapy (CRT) is used to improve cognitive functioning in patients with Schizophrenia Spectrum Disorders (SSDs). Most of the previous studies had incorporated a long rehabilitation program. This study aimed to evaluate the effects of a short and easy to implement computer-based CRT on cognitive performance in patients with SSDs using a randomized controlled trial design.

Sixty-Two patients with SSDs were enrolled in Roozbeh Hospital (Tehran City, Iran); they were randomized to either receive a CRT program added to the standard pharmacological treatment (n=31) or the standard treatment alone (n=31). The remediation consisted of 10 sessions of CRT provided 2-3 times a week applying the Cogpack software. The cognitive performance was assessed in attention, memory, and executive functions before and after the intervention using the respective tests of the Cambridge Neuropsychological Test Automated Battery (CANTAB).

This study did not demonstrate any significant improvement in attention and executive function between the experimental and control group. However, we observed modest improvements in some aspects of visual memory (first trial memory score, F=9.152, P<0.001, Cohen’s d=0.40; mean errors to success, F=6.991, P=0.011, Cohen’s d=0.14; stages completed on the first trial, F=7.155, P=0. 010, Cohen’s d=0.71; total errors, F=5.730, P=0.020, Cohen’s d=0.53).

We observed only modest improvements in the patients’ cognitive functioning after a short course of CRT. The short duration of the training and lack of a comprehensive rehabilitation plan may explain the obtained findings.

Allan-Herndon-Dudley Syndrome (AHDS) is a rare X-linked recessive intellectual disability condition with neuromuscular involvements. Altered thyroid function tests are major milestones in AHDS diagnosis. However, due to phenotypic variations in the levels of thyroid hormones in AHDS patients, we believe that the disorder is often underdiagnosed. Here, we reported a 3.5-year-old boy with an AHDS diagnosis and healthy thyroid hormones.

Whole-Exome sequencing followed by data analysis was performed on the patient’s sample. The mutation was confirmed by Sanger sequencing in the patient and his mother.

We reported a 3.5-year-old boy with AHDS diagnosis and a novel synonymous missense mutation (c. 1026G>A) in the SLC16A2 gene manifesting normal levels of T3, T4, and TSH. The mutation causes no change in amino acid sequence; however, it affects splicing through alteration of an exonic splicing enhancer. To the best of our knowledge, there are only 3 similar reports in the literature reporting AHDS diagnosis and normal levels of thyroid hormones.

The altered levels of thyroid hormones are notable but not necessary markers for diagnosing AHDS. The candidate diagnosis of AHDS should be considered in patients with X-linked recessive intellectual disability syndrome with neuromuscular involvements irrespective of levels of thyroid hormones; otherwise, it could lead to the under-diagnosis of the disorder.