10^th International Conference on Neuroscience and Neurochemistry February 27-28, 2017 Amsterdam, Netherlands

Biography:

Rodrigo Pascual has completed his MSc and PhD at Universidad Autónoma de Barcelona School of Medicine (Spain). He has published more than 20 papers in reputed journals and four books.

Abstract:

Several studies have indicated that abnormal prenatal changes in the circulating glucocorticoids (GCs), induced by either maternal stress or exogenous GC administration, significantly alter the development of Purkinje cell (PC) dendrites and synaptogenesis. However, it is unknown whether a single course of a therapeutic dose prenatally GCs alters the major synaptic vesicle protein synaptophysin (Syn). Thus, in this study we analysed whether a single course of prenatally administered betamethasone phosphate (BET) in pregnant rats changes the immunohistochemical expression of Syn along with locomotor behaviour (rota rod-test). The data obtained showed that in utero BET exposure resulted in a significant immunohistochemical underexpression of Syn and a significant reduction in locomotor behaviour during late postnatal life. In conclusion, our previous and current works indicate that prenatal BET administration significantly modify the cerebellar development. Of note, these and other experimental data do not portend to minimize the beneficial effects of BET administration when there is a risk of respiratory distress/bronchopulmonary dysplasia in preterm infants.

Biography:

Ali H Alwadei currently works at Pediatric Neurology Department, National Neuroscience Institute, King Fahad Medical City, PO Box 59046, Riyadh 11525, Saudi Arabia.

Abstract:

Biography:

Masayuki Yamashita is a Professor of Physiology at International University of Health and Welfare. He completed his PhD in Department of Neurophysiology, University of Tokyo in 1986. He moved to National Institute for Physiological Sciences (Okazaki, Japan) as a JSPS Fellow and a Research Associate. In 1989, he started physiological studies of retina in Department of Neuroanatomy, Max-Planck-Institute for Brain Research. After the reunification of Germany, he moved to the Department of Physiology, Osaka University Medical School. He studied the calcium signaling systems in embryonic chick retina. Then, he moved to the Department of Physiology, Nara Medical University as a Professor (1999-2014). He has been interested in “The electrophysiological properties of neuroepithelial cells and newborn neurons”. The retina is a nice model for studying the early development of central nervous systems.

Abstract:

The axons of embryonic brain, spinal cord and retina extend along the extracellular voltage gradient towards the cathode in a process known as galvanotropism. In embryonic nervous tissues, positive direct current (DC) potentials are generated by neuroepithelial cell’s sodium transport, of which disruption results in erroneous axon path-finding, suggesting that electric fields play a pivotal role in orienting newborn axons. However, the experimental evidence was lacking for the cell surface molecule that is activated asymmetrically in an electric field. Here, it is shown that integrin activation mediates electric axon guidance. Retinal strips of chick embryos were embedded in Matrigel®, and cultured in the electric field of the same strength as that in vivo (15 mV/mm). Matrigel® contained the same extracellular matrix proteins as in the embryonic retina, laminin and collagen, to which integrins bind. Retinal ganglion cell axons extended towards the cathode. A monoclonal anti-chicken integrin antibody (TASC), which enhances integrin-ligand binding, accelerated the cathodal growth. A reduction in the extracellular free Ca²⁺with EGTA also enhanced the cathodal growth, which suggested that millimolar Ca²⁺ inhibited axon growth, and also that the influx of Ca²⁺ was unlikely to be essential for cathodal steering. In the presence of Mn²⁺, which non-specifically activates integrin-ligand binding, the axons formed local meshes. These results suggested that the inhibition of integrins by the extracellular Ca²⁺ underlies electric axon guidance.

Biography:

Abstract:

Various groups have presented findings that human mesenchymal stem cells (MSCs) have both immunomodulatory and trophic properties. MSCs tend to act indirectly at sites of injury or damage through the secretion of paracrine factors in vitro and in vivo. For example, our studies have been done using a transgenic Alzheimer’s disease mouse model where intraparenchymal injections of MSCs resulted in the reduction of amyloid plaque levels, anti-apoptosis, and activation of endogenous neural stem cell and also activate proteasome in neuron. In addition, efficient MSC delivery is also a significant issue for human study. By possessing a broad range of functions, MSCs hold great potential in being used as a novel treatment for various diseases including neurodegenerative disorders.

Biography:

Eva Kudova has been working at Institute of Organic Chemistry and Biochemistry in Prague, Czech Academy of Sciences (IOCB) since 2002. She completed her PhD in 2009 at Charles University in Prague. Then, she worked for two years in the lab of Douglas F Covey at Washington University School of Medicine in St. Louis, Missouri, USA. Since 2011, she works at IOCB as the Project Investigator (PI) at Targeted Research Group of Steroidal Inhibitors. Her main research interest is Steroidal Chemistry. She has been working in this field for more than 10 years. Her major avenue of investigation is design and synthesis of new neuroactive steroidal compounds and structure-activity relationship studies affording NMDARs ligands.

Abstract:

Neurosteroids are compounds synthesized in the nervous tissue from cholesterol or steroidal precursors from peripheral sources. It is believed that neurosteroids execute their effects by modulating the activity of different membrane receptors, including the glutamatergic ionotropic receptors, e.g. N-methyl-D-aspartate receptors (NMDARs). The NMDARs play an important role in development, synaptic plasticity, learning and memory, however, abnormal activation of NMDA receptors have been shown to mediate neuronal degeneration/cell death. To find novel potentially beneficial drugs to treat neurological damage or neuro-degeneration is one of the most investigated areas in contemporary pharmacology and neuroscience. Therefore, we have designed and synthesized a library of SMART steroids- steroidal molecules as rapid-acting therapeutics. SMART steroids are neuroactive molecules, targeting primarily NMDARs, show neuroprotective properties and minimal side effects in animal models. Our screening pipeline currently covers physicochemical and biological properties like: Solubility (DLS); lipophilicity (logP, logD, ΔG_solv); patch-clamp recordings from HEK293 cells assessing NMDAR inhibition rates and IC₅₀ values; caco-2 assay, treatment of glutamate and NMDA-induced neurotoxicity (survival rate, caspase-3, intracellular calcium levels, ROS); in vitro growth of postnatal neurons after neurosteroid administration; models of animal behavior (open field, elevated plus maze, forced swim test, etc.); PTZ-induced seizures; paclitaxel-induced peripheral neuropathy and; pharmacokinetic properties. Our results indicate that these compounds do afford neuroprotective effect and as such, SMART steroids may be beneficial in treatment of several neurological diseases like epilepsy, neuropathic pain, AD, PD and others. Broad patent portfolio has been developed protecting compounds, production and its use for treatment in neurology etc.

Biography:

Mohamed Shaban is currently working at Cairo University as a special surgeon from the year 2009 to 2017. He has many research works published.This is one of the latest research he submitted to the university.

Abstract:

Object: Adjacent-segment failure is a well-known risk of lumbar fixation. The aim of this retrospective study was to identify risk factors for next-segment failure in lumbar fixation for degenerative instability.

Method: We retrospectively evaluated 122 patients who underwent of lumbar fixation for degenerative instability from 2011 to 2014 in Faculty of Medicine, Cairo University. All procedures were performed by a single surgeon. The patients with next-segment failure underwent neurological assessment, radiographic studies and sequential follow-up examinations. The mean follow-up period for this group was 30 months.

Results: 33 patients of 122 fusion procedures were performed in women who were postmenopausal. A total of 19 patients of 125 patients developed symptomatic next-segment degeneration at a previously asymptomatic level; 15 were postmenopausal women. All women were postmenopausal, and 50% received bisphosphonate drugs and calcium supplementation preoperatively for osteopenia. 20% of all patients with next-segment failure were cigarette smokers. Next-segment diseases included spondylolisthesis (52%), spinal canal stenosis due to disc herniation and/or facet hypertrophy (33%), stress fracture (12%), and scoliosis (3%). Patients may have more than one degenerative process at the next segment.

Conclusions: Postmenopausal women show the highest risk of adjacent-segment failure for patients in whom lumbar fusion with rigid instrumentation is performed to treat degenerative instability.

Biography:

Getachew Desta completed his Doctor of Medicine at Gondar University and has one and half years of working experience as a Lecturer at Bahir Dar University. Currently, he is a fourth year Resident in Surgery at Bahir Dar University.

Abstract:

Background: Craniopagus parasiticus is a rare medical case and it is unique unlike other cases reported from different literature. The head of parasitic twins is protruding from the temporal area of cranium. Parasitic head has two deformed lower limbs; one is too rudimentary attached to the mass; long bones of bilateral lower limbs and some pelvic bones. After dissection of the mass, the intestine was seen but no chest organs and other abdominal organs. There is also rudimentary labium but no vaginal opening.

Case Presentation: A 38-years-old multigravida (gravida V para IV) women from Amhara ethnicity referred from rural health center to referral hospital due to prolonged second state of labor at 42+1 weeks. Upon arrival, she had contraction, term sized gravid uterus, and fetal heart beat was 112. On digital pelvic examination the cervix was fully diluted, station of the head was high and the pulsating umbilical cord coming in front of the presenting part with ruptured membrane but yet in the vaginal canal. The team decided emergency cesarean section and then a live female infant weighing 4200 g was delivered. The placenta was single and normal. The APGAR scores were seven and nine at one and five min, respectively. The infant appeared to be grossly normal except the parasitic co-twin attached at the cranium. The neonate was investigated with the available investigations (CBC, X-Ray, Doppler ultrasound) and pediatric side consultation made. After a week of counseling and investigations, successful separation operation was done. During post-operative time the neonate comfortably suckling on breasts and no neurological deficit. The details of the surgery, post- operative condition & subsequent follow up will be discussed during the conference.

Conclusion: The possible etiologies of craniopagus parasiticus are still unknown due to a rarity of cases. Doctors, genetic scientists, epidemiologists and researchers continue to investigate this case as the reasons that could give clue to birth defect and to provide answer for better prognosis of cases and improve the life chances of the twins. This case will have some input in the effort to know the etiology and pathogenesis of this new borns.

Biography:

Abstract:

Biography:

Paula Kielbik is currently a PhD student at Warsaw University of Life Sciences, Faculty of Veterinary Medicine. She completed both her Bachelor Degree and Master of Science Degree under supervision of Dr Michal Godlewski in Nanotechnology laboratory in collaboration with Polish Intitute of Physics. In her scientific work, she focused mainly on “Biodistribution of biodegradable nanoparticles in the living organism”. The main aspect of her work was transfer of nanoparticles through the organism barriers (i.e. intestinal barrier, blood-brain barrier, blood-testis barrier) by ZnO-derieved NPs in adult organism. Working as a member of a team in Nanotechnology laboratory, she was involved in the development and assessment of compherehesive methodology for the evaluation of gastrointestinal absorption, circulation and elimination from the organism of biodegradable nanoparticles.

Abstract:

Zinc oxide nanaoparticles (ZnO NPs) became promising material for numerous applications, including biomedicine. Avaible reports assessing their biodistribution present contradictory conclusions. Furthermore transfer of NPs through the blood-brain barrier has not been reported extensively. In our study, we orally administrated fluorescent. ZnO NPs doped with Europim (ZnO:Eu) to mice (n=35). After 3 h, 24 h, 7 d, 14 d or 1 m mice were sacrificed and internal organs were collected for the assessment of biodistribution and localization of NPs in the organism. For the analyses, we proposed a novel comprehensive and innovative approach. Along with the measurement of Zn concentration in organs with spectroscopy method (AAS), we performed quantitative and qualitative cytometric evaluation of collected samples. The distribution patterns of ZnO:Eu NPs within tissues were statistically assessed with scanning cytometry, while the extent of biodegradation was semiquantitatively elucidated by confocal microscopy. Results revealed very rapid and efficient uptake and distribution of ZnO:Eu NPs to key organs and tissues, also crossing physiological barriers. Spleen, as well as fat tissue were responsible for accumulation of NPs, and liver with kidney were designated for their elimination. An interesting pattern of biodistribution of NPs in the brain was also observed. Following 3 h after IG administration, we observed crossing of the blood-brain barrier by ZnO:Eu NPs and their uniform distribution in the brain. Similar observations were reported earlier for non-biodegradable ZrO₂:Pr NPs and Y₂O₃:Eu NPs. The peek of NPs transfer to the brain seems to take place 24 h post IG with majority of NPs allocated in the areas of dense neuronal networks, limbic system and cerebellum. During following days, we observed a drop of NPs-related fluorescence. However, the association with limbic system and dense neuronal networks remained. We speculate that elimination of the NPs from the brain might be consequential of biodegradation of NPs and their efficient elimination via neuronal transport.

Biography:

Ramel A Carlos is a Board Certified Neurologist. He is currently working at Neurology Clinic in Tamuning, Guam. He completed his Residency and fellowship training at Wake Forest University, Winston-Salem, North Carolina.

Abstract:

Emerging evidence suggested a link between Obstructive Sleep Apnea (OSA) and cognitive decline, including dementia. The severity of cognitive impairment has been reported to be directly correlated with the degree of OSA. Neurodegenerative changes and vascular diseases are significant comorbidities on these patients. We report the occurrence of OSA in patients with dementia in the Island of Guam and to correlate the severity of OSA with the results of the neuropsychological testing and neuroimaging studies. We also report the prevalence of comorbid vascular diseases in these patients. A retrospective analysis of medical records of patients evaluated at Neurology Clinic with the diagnosis of OSA and dementia from August 2006 to June 2016 was conducted. There were 359 patients with dementia and 17% have been diagnosed with OSA. Among patients with OSA, 45% have moderate to severe OSA with moderate degree of cerebral atrophy on the neuroimaging studies and 17% have mild OSA with mild degree of cerebral atrophy. 17% of patients with moderate to severe OSA have moderate impairment on global cognitive scores and 17% with mild OSA have mild impairment on global cognitive scores. 25% of patients with moderate to severe OSA have stroke and 17% have leukoaraiosis in the neuroimaging studies. The prevalence of vascular diseases on patients with moderate to severe dementia showed that 75%, 58%, 66% and 33% of patients have hypertension, diabetes mellitus, hyperlipidemia and heart diseases, respectively, Wherein patients with mild dementia, hypertension, diabetes mellitus, hyperlipidemia and heart diseases were identified on 70%, 54%, 60% and 30% of patients, respectively. Conclusion: OSA is a common sleep disturbance in patients with dementia. The severity of OSA correlates closely with the degree of cerebral atrophy and global cognitive scores. Various comorbid vascular diseases are frequently encountered in patients with OSA and dementia. 

Biography:

Boon Chuan Low is a Principal Investigator at Mechanobiology Institute and Department of Biological Sciences, National University of Singapore. His research work focuses on “Defining cellular and molecular mechanisms underlying neuronal differentiation and cancer metastasis”. His discovery on the BCH domain as a versatile protein scaffold has led to our better understanding of the intricate spatiotemporal regulation of GTPases, kinases and metabolic signaling in cell morphogenesis, cell motility, cell growth and differentiation. His work also extends to BCH and other scaffold proteins that can integrate both biochemical and mechanical signals in cell-cell and cell-matrix interaction, leading to tissue organization and organogenesis.

Abstract:

The neurotransmitter acetylcholine (ACh) is essential for neuron development, memory, learning and motor movement. It is synthesized from choline and acetyl-CoA by choline acetyl transferase (ChAT). ATP citrate lyase (ACL) is a key metabolic enzyme that produces the acetyl-CoA for this process. However, the precise spatial disposition of this cholinergic machinery for both morphogenesis and neurotransmission remain largely unknown. Mutations in the ATCAY/Atcay gene, which encodes a BCH domain containing BNIP-H (also known as caytaxin), lead to ataxia and mental retardation in humans (cayman ataxia), as well as ataxia and dystonia in several rodent models. Recently, we used molecular genetics, biochemical and imaging methods and revealed that BNIP-H recruits the cholinergic machinery to neurite terminal to regulate cholinergic signaling. BNIP-H links kinesin-1 (KLC1) motor protein to ACL and transports ACL towards neurite terminal. Therefore, the BNIP-H/ACL complex synergistically recruits ChAT, leading to enhanced secretion of ACh. ACh then activates MAPK/ERK via muscarinic receptors to promote neuritogenesis. In mice deficient in BNIP-H, ACL fails to interact with KLC1, and formation of the ACL/ChAT complex is prevented. Significantly, Bnip-h knockdown in zebrafish causes axon defect of motor neuron through impaired cholinergic pathway, leading to motor disorder. Here, we further show that BNIP-H specifically engages Rab11 GTPases and a component of the actin-based exocyst complex to regulate its dynamic disposition and neurologic function. In conclusion, BNIP-H promotes cholinergic signaling by trafficking ACL to neurite end, where ChAT is subsequently recruited to regulate the local production of ACh. Our results provide the first molecular evidence that precise spatial regulation of the cholinergic machinery is crucial in neuronal differentiation and neurotransmission, the significance of which will be further discussed.

Biography:

Seyyedeh Elaheh Mousavi is an Assistant Professor of Pharmacology at Tehran Medical Science University. He has worked in different fields of Pharmacology in various in vivo and in vitro models. Currently, he has published more than 10 articles in the renowned journals of pharmacology.

Abstract:

Testicular torsion/detorsion (T/D) can induce depression in pre- and post-pubertal patients. This study was conducted to investigate the psychological impact of testicular torsion and mechanism underlying its depressive-like behavior, as well as antidepressant-like activity of minocycline and possible involvement of nitric oxide (NO)/cyclic GMP pathway in this paradigm in male rats undergoing testicular T/D. Unilateral T/D was performed in 36 male adult Wistar rats, and different doses of minocycline were injected alone or combined with Nx-nitro-L-arginine methyl ester (L-NAME), non-specific NO synthase (NOS) inhibitor; aminoguanidine (AG), specific inducible NOS inhibitor; L-arginine, an NO precursor; and selective PDE5I, sildenafil. After assessment of locomotor activity in open-field test, immobility times were recorded in the forced swimming test (FST). Moreover, 30 days after testicular T/D, testicular venous testosterone and serum nitrite concentrations were measured. A correlation was observed between either a decrease in plasma testosterone or an increase in serum nitrite concentrations with prolongation in immobility time in the testicular T/D-operated rats FST. Minocycline (160 mg/kg) exerted the highest significant antidepressant-like effect in the operated rats in the FST (p<0.001). Furthermore, combination of sub-effective doses of minocycline (80 mg/kg) and either L-NAME (10 mg/kg) or AG (50 mg/kg) demonstrated a significant robust antidepressant-like activity in T/D group (p<0.01). Consequently, NO/cGMP pathway was involved in testicular T/D-induced depressive-like behavior and antidepressant-like activity of minocycline in the animal model. Moreover, a contribution was observed between either decreased testosterone or elevated serum nitrite levels and depressive-like behavior following testicular T/D.

Biography:

Azam Bakhtiaran has her expertise in Pharmacology. Her main research focus is on “Characterizing effect of different drugs on both in vitro and in vivo models. She has completed her PhD at University of California in Irvine and she is currently an Associate Professor of Pharmacology at Tehran University of Medical Sciences

Abstract:

Evidence show that gamma-aminobutyric acid (GABA) receptors are involved in depression, so the aim of this study was to investigate the effect of nitrazepam as agonist of GABAA receptors on depression and curiosity in male mice and the role of potassium channel in antidepressant-like response. For this purpose, we studied the antidepressant-like properties of fluoxetine, nitrazepam, glibenclamide, and cromakalim by both forced swimming test (FST) and tail suspension test (TST). Animals were injected by various doses of nitrazepam (0.05, 0.1, and 0.5 mg/kg). Nitrazepam at dose of 0.5 mg/kg significantly decreased the immobility time compared to control group in both FST and TST. Fluoxetine also showed such a response. Co-administration of nitrazepam (0.05 mg/kg) with glibenclamide in TST (1 mg/kg) and in FST (0.3, 1 mg/kg) also showed antidepressant-like response. Beside, cromakalim (0.1 mg/kg) could reverse the antidepressant-like effect of nitrazepam (0.5 mg/kg) in both FST and TST, while cromakalim and glibenclamide alone could not change the immobility time compared to control group (P40.05). The hole-board test revealed that nitrazepam at doses of 0.5 and 0.1 mg/kg could increase the activity of the animal’s head-dipping and boost the curiosity and exploration behavior of mice. The results of this study revealed that nitrazepam may possess antidepressant-like properties and this effect is dependent to potassium channels in both FST and TST.

Biography:

Farahnaz Jazaerijooneghani has completed his MD and PhD at Tehran University of Medical Sciences. She has been Assistant Professors at Tehran University of Medical Sciences, Pharmacology department since 2013. She has published more than 10 papers in reputed journals and presented posters in EASL Congress (Europe) and Pharma Nutrition Congress in Philadelphia. She has supervised and advised more than 10 medical students, masters and PhD students.

Abstract:

Cirrhosis is associated with cardiac chronotropic and inotropic dysfunction which is known as cirrhotic cardiomyopathy. Cardiac responsiveness to adrenergic stimulation is impaired in cirrhosis. Moreover, there is vagal nerve dysfunction which is related to neuromodulatory dysfunction of the angiotensin II in the cirrhosis. This study was aimed to explore the hypothesis that administration of losartan-angiotensin II receptor antagonist- increases cardiac chronotropic response to isoproterenol in cirrhotic rats; and if so, whether this is associated with altered cardiac TGF-β receptor expression. Cirrhosis was induced by surgical ligation of the bile duct (BDL) in male Wister rats. Half of the BDL-group and control group were treated with losartan for four weeks. Four weeks after bile duct ligation or sham surgery the atria were isolated and spontaneously beating rate and chronotropic responsiveness to β-adrenergic stimulation was assessed using standard organ bath. Pathological assessment was done on the atria. Moreover, the expression of TGF-β was assessed the atria using quantitative RT-PCR. Bile duct ligation could induce a significant hypo-responsiveness to adrenergic stimulation. In cirrhotic rats, the chronotropic responses increased after chronic treatment with losartan but it was not significant. Pathological study showed that losartan decreases fibrosis in atria in losartan treated cirrhotic group. TGF-β expression is markedly increased in cirrhotic rats which are significantly decreased in atria following administration of losartan. These results might be considered as angiotensin II role in cirrhotic cardiomyopathy but further studies are required to elaborate the mechanism as well as possible advantage of losartan. We conclude that cirrhosis in rats is associated with altered expression of TGF-β in atrium which losartan can ameliorate it.