1Semnan University of Medical Sciences, Iran
2Monash University, Australia
Poor postural stability and balance impairment are common problems in older adults with high falls risk. Preventive interventions to decrease falling rate in aging population is important. The aims of this study were to investigate the short-term and long-term effects of cerebellar anodal transcranial direct current stimulation (a-tDCS) on postural stability and balance in older individuals with high falls risk.
Twenty nine older adults with high falls risk were randomly allocated into two groups of experimental (n=15) or sham tDCS group (n=14). Cerebellar a-tDCS was applied for 20 minutes with 2 mA in experimental group. The berg balance scale and the anterior-posterior, medial-lateral and overall stability indices in both static and dynamic levels of Byodex Balance System (BBS) were assessed before, immediately after and one-week after the intervention.
The results indicated no changes in postural indices and balance immediately or one-week after a-tDCS intervention in experimental group (P>0.05). In addition, there were no significant differences in postural stability indices or balance between groups (P>0.05).
This study showed that one-session cerebellar a-tDCS could not improve postural control or balance in older individuals with high falls risk.
Keywords: Older adult, high fall risk, Transcranial direct current stimulation, cerebellum, balance
Biography:
Fatemeh Ehsani is the faculty member of Neuromuscular Rehabilitation Research Center, Semnan University of Medical Sciences, Semnan, Iran. Her academic degree is PhD of physiotherapy and is working as assistant Professor. Her research fields are motor control and motor behaviors, clinical neuroscience intheageing and neurological disorders. Thirty-six papers are published in these fields by her and her colleagues. The current study was also investigated about the effect of CNS modulator (tDCS) on posture and balance of older adults with high falling risk.
University of Glasgow, UK
Our laboratory at UCL Institute of Neurology investigates the use of olfactory ensheathing cells (OECs) for the repair of spinal cord injury. These specialised glia usually function to guide new olfactory axons as they pass from the periphery and terminate within the olfactory bulb. Over a number of years, we have shown that in experimental spinal cord injury models, OECs promote long-distance regeneration along with restoration of functions such as grasping and breathing.
We have developed a dorsal root transection model to mimic a brachial plexus injury such as may occur after a motorbike crash. We transplanted olfactory bulb OECs into a unilateral rhizotomy injury at the cervical level and found a return of proprioception in a climbing test. With a similar model, we demonstrated that transplanting OECs prevented abnormal forepaw sensations to hot or cold stimuli. This has important clinical implications.
Most recently we have transplanted human OECs within a collagen scaffold into the rat spinal root injury model. Half of the transplanted animals showed a return of climbing function. This setup allows us to test and optimise human OEC culture methods and the use of biomaterials to fill cavities that are common after injury.
Biography:
Mr. Andrew Collins has completed my undergraduate degree in neuroscience at Glasgow University before going to Bristol University for a PhD. The focus of this doctorate was the mechanisms underlying improved stress-coping following voluntary exercise in rats. The surgical techniques and behaviour tests which allowed a systems level approach enabled me to switch to the field of spinal cord repair. I have been a post-doctoral researcher at UCL since 2012, using specialised glia called olfactory ensheathing cells to repair injury in a rat model of brachial plexus injury. Translating basic research into better treatments in the clinic is my primary goal.
King Abdul Aziz University, Saudi Arabia
Introduction: High fat diet (HDF) increases the risk of developing molecular inflammation in the central nervous system (CNS). Recently, several herbal extracts have been investigated for its protective effect when consuming HFD. Nigella sativa (NS) have significant anti-inflammatory and anti-oxidant proprieties and it could be a novel neuroprotective agents.
Objectives: this study designed to evaluate the neuroprotective effect of NS seeds on the brain inflammatory cytokines and the histopathological changes in the cerebellum of rats fed HFD and treated with NS.
Methods: Fifteen male rats were randomly divided into three groups: 1st group, fed normal diet, 2nd group, fed high saturated fat diet (SFD) at a dose of (6ml/day) for 8 weeks, 3rd group, fed SFD for 4 weeks then added NS at a dose of (300mg/kg/day) for 4 weeks. Blood samples were collected to measure brain inflammatory cytokines IL-1β, IL-6 and IL-10 using multiplex technique and brain samples for histopathological examination.
Results: Pro-inflammatory cytokines (IL-1β, IL-6) were elevated in comparison to NS treated and control groups ****p < 0.0001, **p < 0.01 respectively. In contrast, anti-inflammatory cytokine IL-10 level was decreased in HFD group ***p < 0.001 in comparison to NS treated and control groups. Indicating a significant improvement by the treatments with NS. Histopathological examination of cerebellar sections showed sings of purkinje cells inflammation in the HFD group.
Conclusions: Nigella sativa could serve as an effective neuroprotective agent due to its anti-inflammatory action seen in the treated group.
Naju National Hospital, Korea
Objective: The purpose of this study was to investigate the efficacy and tolerability of blonanserin in schizophrenic patients who used other atypical antipsychotics (AAP) and switched to blonanserin due to inadequate responses or unwanted drug effects.
Methods: A total of 63 patients (male=33, female=30) with schizophrenia who were partially or completely unresponsive (N=52 (82.5%)) or intolerable to treatment with existing AAP (N=11 (17.5%)) were recruited in this 12-week, open-label, prospective study. Blonanserin was cross-titrated for 2 weeks. Efficacy was evaluated using the Brief Psychiatric Rating Scale (BPRS), Social and Occupational Functioning Assessment Scale (SOFAS). Tolerability was also evaluated using Abnormal Involuntary Movement Scale (AIMS), Barns Akathisia Scale (BARS), Simson Angus Rating Scale (SARS). All assessments were done at baseline, weeks 1, 2, 4, 8, and 12.
Results: Among 63 patients, premature discontinuation occurred in 22 patients (34.9%); 6 of these patients were dropped out due to adverse events. Switching to blonanserin was effective and well-tolerated in both group. The BPRS total score was significantly decreased at 12 weeks after switching to blonanserin in both unresponsive group (-15.3±14.4, p<0.001) and intolerable group (-2.81±5.1, p<0.001). The SOFAS total score was significantly increased in unresponsive group (7.1±11.1, p<0.001), but not in intolerable group (-1.0±7.5, p=0.639). There were no significant differences between baseline and any assessment points on SARS, BARS, AIMS scores in both group.
Conclusion: These results showed that switching to blonanserin could be an effective strategy for schizophrenic patients who were unresponsive or intolerable to other atypical antipsychotic treatments.
Biography:
Dr. Bo-Hyun Yoon is a Korean psychiatrist who is working at a national mental hospital. He is a vice-president of the Korean College of Neuropsychopharmacology (KCNP) and president of the Korean Society of Affective Disorder (KSAD). His major interests are Psychopharmacology and mood disorders
Tashkent Medical Academy, Uzbekistan
It is known that, in vascular parkinsonism and Parkinsonʼs disease it is observed shortening of steps, bradi, oligokinesis, and also tremor disturb such kind of patients Despite, there have been developed several methods in order to differentiation, diagnostics and effective treatment maintaining to be one of the most important topics of the nowadays.
Methods of Research: In order to early and effective differential diagnostics, also to properly treat of tremor and short steps in vascular parkinsonism and Parkinsonʼs disease it is used method of tempo-rythmal correction80 patients have participated in our research and the mean age of them was 62.3 ± 4.7 years. All patients were divided into 4 group:
1st group - patients who have vascular parkinsonism and they have received both medicamentous treatment and temporythmal correction.
In the group 2 were patients with Parkinsonʼs disease, they have also received both medicamentous treatment and temporythmal correction.
Group 3 was a group of patients with vascular parkinsonism they have received only medicamentous treatment.
4th group of patients with Parkinsonʼs disease, they have received also only medicamentous treatment.
First of all, there is measured height, weight and body mass index. Calculated and scheduled common length of steps, amount of steps passed in 500 m and sum of spent kcal. Patients were observed during 10 days: was selected quiet music and have measured amount of steps and length of passed distance for 3 times during the 10 day. Patients walked in the morning under quiet music, on the midday under quickened and on the evening under fast rythm music. The results were recorded while there were walking.
All patients were evaluated by the Parkinsonʼs Disease Questionnaire (PDQ-39) scale.
Results: According to the results of our 10-day observations.
In 1st group the maximal positive result according to PDQ-39 was on “vital activity” and was 2.87 ± 1.36. Patients said that they had felt easiness while dressing, bathing, eating and serving to themselves. In normal people the average length of step is 40% of the height, in the first days of tempo-rythmal correction in all patients this index was 25 or 28% and 30 or 32% on the last day of correction.
In patients of 2nd group according to PQD-39 the maximal positive outcome was on “vital activity” and is 2.23 ± 1.16. Patients of this group said that they felt more easiness on dressing and eating. The average length of steps in patients with Parkinsonʼs disease was 21 or 23% on the first day of the temporythmic correction, and 22,24% in the last days of the temporythmal correction.
Groups 3 and 4 received only medicamentous therapy, and correction was not conducted in group patients. The PDQ-39 consisted in 3rd group - 1.9 ± 2.16 and 4th group - 2.03 ± 1.37.
Conclusion: In conclusion, we can say that temporythmal correction is method of treatment and rehabilitation, which is effective in each type of vascular parkinsonism and Parkinsonʼs disease also in economical aspect that patient can use both in the hospital and in the home. The average length of steps in Parkinsonʼs disease is more shorter than in the vascular parkinsonism. Temporitmal correction is an effective and cost-effective method of differential diagnosis of vascular parkinsonism and Parkinsonʼs disease
1UCAD, Senegal
2Reference Hospital of Dolisie, Congo
Diabetes is a multifactorial pathology implicating a genetic predisposition and metabolic disorders acquired, which leads to the progressive deterioration of the action of insulin secretion. The international epidemiologic dataʼs concerning the prevalence of diabetes show important disparities between the different countries studied. Whereas, it testifies uniformly from a considerable increase of its frequency in the developing countries. The previsions at the world level estimates that the number of diabetic subjects will leave from 171 million in 2000 to 366 million in 2030. This prevalence is generally underestimated because of hyperglycemia can evoluate in a silent way, during numerous years before the diagnosis is being done. The cost of management diabetes posing an important and increase problem in Public health, long term consequences linked to microangiopathy and macroangiopathy of diabetes constitute invalid pathologies and implicates a heavy management of patients. A couple of epidemiologic arguments, clinical and experimental accumulated in the course of the last 10 years, pleads in favor of a disfavourable effect of the inflammation in a low sound of adipose tissue in the up come of diabetes as well as the neuroinflammation responsible for numerous cognitive disorders notably anxiety and memory disorders. To our knowledge, there exist less data of the literature concerning the action of anti-inflammatory on cognitive disorders. In this context, the objective of our study was to evaluate the effect of acetylsalicylic acid on cognitive deficits in diabetic rat, that which could be one of the interesting therapeutic to explore.
Biography:
Eric Gueumekane Bila Lamou is from Cameroon, he has completed his specialization in Clinical Neurology in 2016 at Cheikh Anta Diop University of Dakar/Senegal and he have been awarded of IFCN Africa Scholarship for the year 2017 for Young Clinical Neurophysiologist. Actually he is doing PhD program in Neurophysiology at the same University. He has published some papers in reputed Journals.
Kangwon National University, South Korea
Purpose: Although multiple reports using animal models have confirmed that melatonin appears to promote neuroprotective effects following ischemia/reperfusion-induced brain injury, the relationship between its protective effects and the activation of autophagy in cerebellar Purkinje cells following asphyxial cardiac arrest and cardiopulmonary resuscitation (CA/CPR) remains unclear.
Methods: Rats used in this study were randomly assigned to 6 groups as follows; vehicle-treated sham-operated group, vehicle-treated asphyxial CA/CPR-operated group, melatonin-treated sham-operated group, melatonin-treated asphyxial CA/CPR-operated group, melatonin plus (+) 4P-PDOT (a MT2 melatonin receptor antagonist)-treated sham-operated group and melatonin+4P-PDOT-treated asphyxial CA/CPR-operated group.
Results: Our results demonstrate that melatonin (20 mg/kg, ip, 1 time before CA and 4 times after CA) significantly improved the survival rates and neurological deficits compared with the vehicle-treated asphyxial CA/CPR rats (survival rates ≥ 40% vs 10%). We also demonstrate that melatonin exhibited protective effect against asphyxial CA/CPR-induced Purkinje cell death. The protective effect of melatonin in the Purkinje cell death following asphyxial CA/CPR paralleled a dramatic reduction in superoxide anion radical (O2·-), intense enhancements of CuZn superoxide dismutase (SOD1) and MnSOD (SOD2) expressions, as well as a remarkable attenuation of autophagic activation (LC3 and Beclin-1), which is MT2 melatonin receptor-associated. Furthermore, the protective effect of melatonin was notably reversed by treatment with 4P-PDOT.
Conclusion: In brief, this study shows that melatonin conferred neuroprotection against asphyxial CA/CPR-induced cerebellar Purkinje cell death by inhibiting autophagic activation by reducing expressions of reactive oxygen species, while increasing expressions of antioxidative enzymes, and suggests that MT2 is involved in the neuroprotective effect of melatonin in cerebellar Purkinje cell death induced by asphyxial CA/CPR.
Keywords: Asphyxial cardiac arrest, Autophagy, Cerebellum, Fluoro-Jade B, Melatonin, Purkinje cells, Superoxide anion radical, Superoxide dismutase
Kangwon National University, South Korea
Purpose: Recent studies have shown that obesity and its related metabolic dysfunction exacerbates outcomes of ischemic brain injuries in some brain areas, such as the hippocampus and cerebral cortex when subjected to transient global cerebral ischemia (tGCI). However, the impact of obesity in the striatum after tGCI has not yet been addressed. The objective of this study was to investigate effects of obesity on tGCI-induced neuronal damage and inflammation in the striatum and to examine the role of mTOR which is involved in the pathogenesis of metabolic and neurological diseases.
Methods: Gerbils were fed with a normal diet (ND) or high-fat diet (HFD) for 12 weeks and then subjected to 5 min of tGCI. HFD-fed gerbils showed significant increase in body weight, blood glucose level, serum triglycerides, total cholesterol and low-density lipoprotein cholesterol without affecting food intake.
Results: In HFD-fed gerbils, neuronal loss occurred in the dorsolateral striatum 2 days after tGCI and increased neuronal loss was observed 5 days after tGCI; however, no neuronal loss was observed in ND-fed gerbils after tGCI, as a assessed by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. The HFD-fed gerbils also showed severe activated microglia and further increased immunoreactivities and protein levels of tumor necrosis factor-alpha, interukin-1beta, mammalian target of rapamycin (mTOR) and phosphorylated-mTOR in the striatum during pre- and post-ischemic conditions compared with the ND-fed gerbils. In addition, we found that treatment with rapamycin, a mTOR inhibitor, in the HFD-fed gerbils significantly attenuated HFD-induced striatal neuronal death without changing physiological parameters.
Conclusion: These findings reveal that chronic HFD-induced obesity results in severe neuroinflammation and significant increase of mTOR activation, which could contribute to neuronal death in the stratum following tGCI. Especially, abnormal mTOR activation might play a key role in mediating the obesity-induced severe ischemic brain damage.
Keywords: Obesity, transient global cerebral ischemia, neuroinflammation, mTOR, rapamycin, neuronal death
Kangwon National University, South Korea
Purpose: Fucoidan is a sulfated polysaccharide derived from brown algae and possesses various beneficial activities, such as anti-inflammatory and antioxidant properties. Previous studies have shown that fucoidan displays protective effect against ischemia-reperfusion injury in some organs. However, few studies have been reported regarding the protective effect of fucoidan against cerebral ischemic injury and its related mechanisms.
Methods: Therefore, in this study, we examined the neuroprotective effect of fucoidan against cerebral ischemic injury, as well as underlying mechanisms using a gerbil model of transient global cerebral ischemia (tGCI) which shows loss of pyramidal neurons in the hippocampal cornu ammonis 1(CA1) area. Fucoidan (25 and 50 mg/kg) was intraperitoneally administered once daily for 3 days before tGCI.
Results: Pretreatment with 50 mg/kg of fucoidan, not 25 mg/kg fucoidan, attenuated tGCI-induced hyperactivity and protected CA1 pyramidal neurons from ischemic injury following tGCI. In addition, pretreatment with 50 mg/kg of fucoidan inhibited activations of resident astrocytes and microglia in the ischemic CA1 area. Furthermore, pretreatment with 50 mg/kg of fucoidan significantly reduced the increased 4-hydroxy-2-noneal and superoxide anion radical production in the ischemic CA1 area after tGCI and significantly increased expressions of superoxide dismutase 1(SOD1) and SOD2 in the CA1 pyramidal neurons compared with the vehicle-treated-group. Additionally, we found that treatment with diethyldithiocarbamate (an inhibitor of SODs) to the fucoidan-treated-group notably abolished the fucoidan-mediated neuroprotection in the ischemic CA1 area following tGCI.
Conclusion: In brief, these results indicate that fucoidan can effectively protect neurons from tGCI-induced ischemic injury through attenuation of activated resident glial cells and reduction of oxidative stress following increasing SODs. Thus, we strongly suggest that fucoidan can be used as a useful preventive agent in cerebral ischemia.
Keywords: Fucoidan, transient global cerebral ischemia, neuroprotection, resident glial cell, oxidative stress, superoxide dismutase
Pusan National University Hospital, South Korea
Purpose: Brain magnetic resonance imaging (MRI) in strabismus can provide valuable information about structural abnormality. The aim of this study is to evaluate the usefulness of MRI in children with strabismus.
Methods: We reviewed medical records retrospectively in patients diagnosed with strabismus by ophthalmologist and underwent magnetic resonance imaging (MRI) at Pusan National University Hospital from January 2012 to March 2017. According to MRI results, it was classified as normal and abnormal. To compare the characteristics of infantile strabismus and childhood strabismus, it was divided based on the age of one.
Results: Ninety patients were enrolled, 47(52.2%) males and 43 (47.8%) females, with mean age of 2.19±0.53. Sixty-four patients (71.1%) had normal MRI, whereas 26 (28.9%) patients showed abnormal MRI. Abnormal fundus examination was higher in abnormal MRI group (p=0.008). There was no significant association between the types of strabismus and MRI abnormalities. Infantile strabismus were 46 people (51.1%) and childhood strabismus were 44 people (48.9%). Global developmental delay, speech delay and MRI abnormalities were more common in infantile strabismus than childhood strabismus.
Conclusion: MRI would be helpful to conduct an MRI for accurate diagnosis and treatment when the patients had developmental delay, especially speech development, infantile strabismus, or abnormal fundus examination.
Fayoum University, Egypt
Background: Cerebrovascular ischemic stroke is highly prevalent in the general population andis considered one of the frequent causes of disability and mortality. Insulin like growth factor-1 (IGF-1)is recognized as an important neuro-protective factor against cerebral vascular ischemic insult.
Aim of the work: To study the relationship between serum IGF-1 levels and acute ischemic stroke (AIS) in the Egyptian population.
Patients and Methods: Two hundred patients with first AIS(within the first 24 hours) were subjected to full neurological examination,assessment of stroke severity usingNational Institute of Health Stroke Scale(NIHSS) and measurement of serum IGF-1 levels. The control group included 100 subjects matched for age, gender, and conventional vascular risk factors.
Results: Serum IGF-1 levels were significantly reduced in cases of first AIS compared to control group. Reduced serum IGF-1 level was an independent risk factor for ischemic stroke with cut off value less than 148.3 ng/ml associated with increased AIS risk.
Conclusion: Lower IGF-1 levels are significantly related to risk of ischemic stroke occurrence, independent from other conventional risk factors in the Egyptian population.
Keywords: Ischemic stroke, risk factors, IGF-1.
Biography:
Dr. Sherine El Mously is an assistant professor of Neurology in the faculty of medicine, Fayoum University. She received her masterʼs degree in Neurology in 2004 and her doctor degree in Neurology in 2009 from the Faculty of Medicine, Ain Shams University. Then. she got a PhD degree in Neurosciences from Verona University, Italy. Interested in neuro-immunology and neuro-oncology. Member of the Egyptian Society of Neurology, Psychiatry and Neurosurgery (ESNPN), the Society of Neuroscientists of Africa (SONA) and the International Brain Research Organization (IBRO)
Sun Yat-Sen University, Peopleʼs Republic of China
Neuroinflammation plays a pivotal role in the incidence and progression of Alzheimerʼs disease (AD). Cathelicidin-related antimicrobial peptide (CRAMP) is critically involved in the innate neuronal responses of chronicneuroinflammation in the AD and thus plays a key role in the disease. Here, we show that Aβ42 induced microglialproduction of CRAMP, which was effectively inhibited by milk-fat globule-epidermal growth factor 8 (MFG-E8). Production of CRAMP was associated with activation of ERK1/2, p38, and phospho-P65-NF-kB upregulation. Additionally, the phosphorylation of these signaling proteins was also reversed by MFG-E8. Pre-incubationwith signaling inhibitors confirmed that MFG-E8 has a regulatory role on CRAMP through MAPK and NF-kBsignaling pathways. MFG-E8 treatment may thus be a potential pharmacotherapy for chronic inflammation in the AD.
Sun Yat-sen University, Peopleʼs Republic of China
Activated microglia are classified into two specificstates: classically activated (M1) and alternatively activated(M2) subtypes. It is believed that the polarization of M1/M2phenotype plays an important role in Alzheimerʼs disease(AD). However, the mechanisms regulating this process remain unclear. Thus, we addressed this question focusing on milk fat globule epidermal growth factor 8 (MFG-E8). MFGE8is a unique protein which can bind to microglia and regulateits inflammatory responses. It is speculated that it mightplay a role in the balance of microglial polarization. In thecurrent study, we used fibril Aβ42 in vitro to stimulate mouseprimary microglial cultures and found subsequent M1 marker expression, along with retained M2 marker production. Then,we discovered that MFG-E8 pretreatment reversed the increased trend of M1 markers and the decreased expression of M2 markers, which were induced by Aβ42. Moreover, MFG-E8 effects could be effectively blocked by an MFGE8 antibody. Further analysis on the signaling pathways showed that NF-κB upregulation and Akt down regulation inmicroglial cultures were observed after Aβ42 incubation. And the alteration of these pathways could also be reversed by MFG-E8. We then assessed the effects of NF-κB and PI3KAkton M1/M2 alteration using their specific inhibitors. Pyrrolidine dithiocarbamate, a NF-κB inhibitor, inhibited M1 marker expression; moreover, LY294002, an Akt inhibitor,enhanced M1 marker expression. Our study indicated the regulatory role of MFG-E8 on microglia M1/M2 alteration forthe first time, providing a basis for understanding the potential role of microglia activation in AD
Contact us for any additional information - contact@madridge.org
Madridge Publishers is licensed under a Creative Commons Attribution 4.0 International License.