Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4th International Conference on Epilepsy & Treatment Zurich, Switzerland.

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Scientific Program Day 1
Scientific Program Day 2

Day 1 :

Keynote Forum

Alain L Fymat

International Institute of Medicine and Science, USA

Keynote: A disrupted blood brain barrier may allow potentially new epileptic treatments

Time : 09:30-10:10

Conference Series Epilepsy 2018 International Conference Keynote Speaker Alain L Fymat photo
Biography:

Alain L Fymat is a Medical-Physical Scientist and an Educator who was educated at the Universities of Bordeaux and Paris-Sorbonne, France, and the University of California at Los Angeles. He is the Current President/CEO and Professor at the International Institute of Medicine & Science. He was formerly Professor of Radiology, Radiological Sciences, Radiation Medicine (Oncology), Critical Care Medicine, and Physics at several US and European Universities. His current research interests lie at the interface between science and medicine (Neurological Disorders; Precision Medicine; Nanobiotechnology; Nanomedicine; Genetics/Epigenetics/Ecogenetics; and Drug Delivery across the brain protective barriers). He has extensively published ~350 scholarly publications and lectured in several national and international academic, professional, governmental and industrial venues. He is a Board Member of several institutions, and Editor-in-Chief, Honorable Editor or Editor of twelve scientific journals.

Abstract:

There are approximately 400 known neurological disorders (including some which may be better classified as mental disorders). Some of these disorders may be due to a disruption or failure of the blood brain barrier (BBB) such as, importantly, epilepsy (a group of neurological disorders characterized by chronic or acute seizures caused by inflammation). Epileptic seizures are the result of excessive and abnormal nerve cell activity in the brain cortex. As of 2015 about 39 million people have epilepsy with nearly 80% of the cases occurring in the developing world and 125,000 having died of it. Common among older people, epilepsy will become more prevalent as a result of the growing aging population. The cause of most cases of epilepsy is still unknown through a process known as epileptogenesis. Nonetheless, there are both genetic and acquired causes, with interaction of these factors in many cases. To date, nearly all the genes discovered to be involved in human epilepsies encode subunits of ion channels, both voltage-gated and ligand-gated. Known genetic mutations are directly linked to a small proportion of cases. Established acquired causes include serious brain trauma, stroke, tumors, infective lesions, and birth defects. Seizures are controllable with medication in about 70% of cases. Inexpensive options are often available. In those whose seizures do not respond to medication, surgery, neurostimulation, or dietary changes may be considered. In its integral form, the BBB is a selective filter that allows passage of essential nutrients, water, some gases, lipid-soluble molecules, hydrophobic molecules (O2, CO2, hormones) and also allows transport of metabolic products to the brain (glucose with specific proteins). It restricts diffusion of microscopic objects (e.g. bacteria) and large hydrophilic molecules and prevents entry of polar and lipid-insoluble substances, and lipophilic neurotoxins. Of interest here are those epileptic treatments rendered possible by the delivery of therapeutic drugs through the disrupted blood brain barrier.

 

Break: Networking & Refreshments 10:10-10:30 @ Europa Foyer

Keynote Forum

Chandramohan Wakade

Augusta University, USA

Keynote: Niacin attenuates inflammatory cytokine upregulation in PD mediated through GPR109A

Time : 10:30-11:10

Conference Series Epilepsy 2018 International Conference Keynote Speaker Chandramohan Wakade photo
Biography:

Chandramohan Wakade has been engaged in the field of CNS injury and its amelioration for number of years. The focus of his research includes trauma to the nervous system and neural repair. He has worked on various animal stroke models including MCAo, SAH and TBI models in rats and mice. His recent work focuses on studying role of inflammation in CNS injury and neurodegenerative diseases in patients.

 

Abstract:

Neuroinflammation is central in Parkinson’s disease (PD) pathology. Microglia derived inflammatory cytokines are known to be involved in progressive degeneration of substantia nigra (SN) neurons. We have demonstrated upregulation of anti-inflammatory receptor GPR109A in blood (PD patients) as well as in SN (post-mortem PD patient samples). Up-regulation of GPR109A may be a part of body’s defense mechanism. Niacin (vitamin B3) acts on GPR109A to reduce the inflammation in PD. To understand the cellular mechanisms involved in the anti-inflammatory action of niacin here we utilize lipopolysaccharide (LPS) induced inflammatory cascade in RAW 267.4 cells. These cells are macrophages that resemble microglial lineage. LPS is known to trigger inflammatory cytokines production such as IL1-b, IL-6 and TNF-a via NF-kB pathway. NF-kB is the transcription factor and the translocation of its p65 unit to nucleus is an essential step in the inflammatory cascade. Here we demonstrate inhibition of pNF-kB translocation by niacin in RAW 267.4 cells via GPR109A. However, in the absence of GPR109A, niacin failed to block the translocation of pNF-kB and the subsequent production of inflammatory cytokines in RAW 267.4 cells. This anti-inflammatory action of niacin via GPR109A might be beneficial in PD to alleviate motor and non-motor symptoms.

 

Keynote Forum

Alcibiades J Rodriguez

NYU School of Medicine, USA

Keynote: Case presentations: sleep phenomena or seizures

Time : 11:10-11:50

Conference Series Epilepsy 2018 International Conference Keynote Speaker Alcibiades J Rodriguez photo
Biography:

Alcibiades J Rodriguez has obtained his Medical degree from the University of Panama, School of Medicine, Republic of Panama. He trained in Neurology at Tuft University, Boston, MA. He completed two fellowships, Clinical Neurophysiology/EEG track and Sleep Medicine at Mayo Clinic Rochester, MN. He is the Medical Director of the NYU Sleep Disorders Center, treating people with epilepsy and sleep disorders using electroencephalography (EEG) and video-EEG monitoring. He is board certified in Neurology, Clinical Neurophysiology, Epilepsy and Sleep Medicine. His research focuses on the effect of seizures and epilepsy on sleep. He has written multiple articles and book chapters related to distinguishing seizures that occur while a person is awake from those that occur during sleep. He has also written about differentiating between a sleep disorder and seizures. He collaborates with the National Institutes of Health on several projects related to sleep and neurodevelopment. He is honorary member of the Sleep-Wake Disorders Study Group of the Spanish Neurological Society, helping to organize and teach an annual sleep medicine course for general practitioners, residents, and fellows. He is Advisor and Consultant for Sleep Medicine for the Neurology and Neurosurgery Institute Prof. Dr. Jose Rafael Estrada Gonzalez, Havana City, Cuba. He has been invited to lecture nationally and internationally. He was Vice Chair of the Lifelong Learning Development Committee of the American Academy of Sleep Medicine and Member of the Education Committee of the World Sleep Society.

 

Abstract:

Background: Epilepsy and sleep are closely related. Not only sleep or lack of sleep can influence EEG and seizures, but seizures can have an impact in sleep consolidation and architecture. Beyond that, the differential diagnosis of nocturnal paroxysmal events include seizures and parasomnias (abnormal sleep behavior). These phenomena may co-exist.

Objective: The goal of the presentation is to discuss different cases of seizures and sleep events, which may overlap or be in the differential diagnosis.

Methods: We will present several video-EEG/sleep cases in order to discuss differential diagnosis of these events. Audience participation will be encouraged.

Conclusion: We hope to clarify similarities and differences, as well as point out strategies to distinguish seizures vs. sleep phenomena.

 

  • Parkinsons Disease | Insights and Therapeutics: Parkinsons Disease | Neurosurgery
Location: Athens
Speaker

Chair

Alain L Fymat

International Institute of Medicine and Science, USA

Speaker

Co-Chair

Jae Moon Lee

Kainos Medicine Inc., South Korea

Session Introduction

Laurice Yang

Stanford University, USA

Title: Diagnosis and treatment for dystonia

Time : 11:50-12:15

Speaker
Biography:

Laurice Yang earned a Master’s Degree in Health Administration at the University of Southern California where she received the high honor as a Dean Merit Scholar. She went on to obtain her Medical Degree from the University of Vermont and completed her Neurology Residency at the University of Southern California where she was appointed Neuroscience Chief Resident and spent the year revamping the entire medical student/resident education curriculum. She completed her clinical training as a Movement Disorders Fellow at the University of California in Los Angeles under Dr. Jeff Bronstein. She is a board-certified Neurologist, specializing in the diagnosis of movement disorders including Parkinson’s disease, atypical parkinsonian disorders, essential tremor, and Huntington’s disease. She has an interest in dystonia and spasticity and has been trained to perform botulinum toxin injection under ultrasound guidance to better ensure accuracy and efficacy with each procedure. She has also presented lectures on topics in dystonia, education, and healthcare administration for CME (Continuing Medical Education) faculty development courses and at the American Academy of Neurology.

Abstract:

Dystonia is a characterized by intermittent, abnormal and often repetitive muscle contractions. The diagnosis of dystonia can often be difficult to assess due to the variability and complexity of the disease. During this lecture, we will first review the historical context of how dystonia was discovered and how the clinical understanding of dystonia had evolved over the last several decades. We will discuss the clinical characteristics of the most common types of dystonia and review how to accurately describe and categorize this very complex disease. We will also review the medical treatment options and discuss the efficacy of botulinum toxin as well as techniques on how to be more accurate during the injection procedure. We will explore the other types of treatment such as sensorimotor retraining therapies, which takes advantage of the neuroplasticity of the brain to help “relearn” normal movement. And lastly, we will explore the surgical options that are available now as well as other types of procedures that could supplement the current treatment options. The learning objectives for this presentation are: Understanding the main diagnostic components of dystonia; being familiar with the different types of dystonia; describing medical and surgical treatment; and describing sensorimotor retraining and its role in those who have dystonia.

Kambiz Hassanzadeh

Kurdistan University of Medical Sciences, Iran

Title: The role of oxidative stress and inflammation in Parkinson’s disease: Current knowledge and future therapeutic strategies

Time : 12:15-12:40

Speaker
Biography:

Kambiz Hassanzadeh is the Associate Professor and Head of Cellular and Molecular Research Center at Kurdistan University of Medical Sciences, Iran. He teaches Pharmacology and Neuroscience courses to Medical and PhD students and does research in the field of Neuroscience with more than 60 publications. During recent years, he has been interested in doing research on molecular nature of neurodegenerative diseases, especially Parkinson’s disease. He also researches on antioxidant agents on animal models of Parkinson’s disease.

Abstract:

Current Parkinson’s disease (PD) therapies are focused on maintaining dopamine levels of brain at normal range. Although, this approach is fairly useful to control and manage Parkinson’s disease symptoms, it has some disadvantages. Previous studies indicate that levodopa and other dopaminergic medications accelerate neuronal degeneration in some parkinsonian brains via production of free radicals and reactive oxygen species (ROS). This is in addition to the main oxidative and inflammatory processes of the PD. Additionally, patients need higher doses of drugs over the time which it implies some serious side-effects including motor and non-motor signs. Oxidative stress and inflammation are considered as the leading cause and progression in many diseases, especially those that are associated with aging such as Parkinson’s disease. During the recent years, interest in administration of neuroprotective factors such as anti-oxidants, anti-inflammatory drugs and neurotrophic factors for management of PD is popularly increasingly. According to the above literature, it is important to understand the mechanism of action of these neuroprotective factors and investigate the new and more effective ones. On the other hand, neuroinflammation is one of the serious complications of PD which is usually developed due to protein aggregates and dopaminergic cell deaths. Therefore, here we review the pathways of these two important aspects of PD (oxidative stress and neuroinflammation) to understand what is happening inside a PD brain and we discuss about the benefit of anti-oxidants and anti-inflammatory drugs based on our recent studies in this area.

Break: Lunch Break 12:40-13:20 @ La Place AB

Byung-Jun Park

Daejeon University, South Korea

Title: HEPAD, a novel therapeutic approach of Parkinson’s disease

Time : 13:20-13:45

Speaker
Biography:

Byung-Jun Park completed his PhD and Korean Doctor in Medicine Degree at the College of Korean Medicine, Daejeon University, Daejeon, South Korea. He has opened a Young Jin Korean Medicine Clinic, and his clinical speciality has been the treatment of Parkinson’s disease and movement disorders since 1995. He has published multiple papers on Parkinson’s disease in reputable journals and is a Member of the Movement Disorder Society. He was listed in the Marquis Who’s Who in the World in 2017–2018.

Abstract:

Parkinson’s disease (PD) is a neurodegenerative disorder involving abnormal body movements. The degenerative loss of dopaminergic neurons in the substantia nigra leads to the onset of PD symptoms, including slow movement, tremor, stiffness, and abnormal posture. Because L-3,4-dihydroxyphenylalanine (L-DOPA) treatment is very effective for symptom inhibition, it is the most widely prescribed treatment of patients with PD. However, long-term L-DOPA treatment is not recommended because of its serious side effects, including dyskinesia. Moreover, L-DOPA does not prevent the progression of PD. Therefore, a novel therapeutic approach is greatly needed for PD. Hepad, a herbal medicine, consists of six Korean medicinal herbs that were selected based on Korean medicine theory. The treatment of patients with PD using Hepad has been clinically effective. In addition, Hepad treatment reduces the required doses of conventional PD drugs, and some patients were able to terminate conventional PD treatments without additional symptom manifestation. A preclinical study has reported that Hepad prevents neuronal cell death by suppressing the production of reactive oxygen species. These neuroprotective effects of Hepad have also been observed in animal experiments. Hepad treatment in a PD animal model increased dopaminergic neuron number and dopamine levels in the substantia nigra to similar or higher levels than those in L-DOPA-treated animals. Considering the complexity of PD, a multi-targeted approach with multiple compounds would be more effective than single-compound treatment. Taken together, these results suggest that Hepad, a mixed Korean herbal medicine, would be an effective treatment for patients with PD.

 

 

D’Auria Stanislao

Ospedale Santa Maria della Misericordia di Udine, Italy

Title: Steering stimulation and directional leads- a recent reliable concept to improve follow-up in implanted patients: A preliminary experience

Time : 13:45-14:10

Speaker
Biography:

D’Auria Stanislao  graduated in Medicine in 2003 did a specialization in Neurosurgery in 2008 from Second University of Naples, School of Medicine. Since 2008, he works as a Neurosurgeon at the Department of Neuroscience of Santa Maria della Misericordia in Udine, Italy. His fields of interests are Functional Neurosurgery and Neuromodulation and Neuro-Oncology. He has published more than eight papers in reputed journals and has been involved in many international congresses.

Abstract:

In the last 20 years, thanks to technological development and still ongoing innovations in features and materials of implantable devices, deep brain stimulation (DBS) has become one of the most effective, reliable and safe surgical procedure for treatment of many different movement disorders.  The clinical condition that has been better treated with such a technique is Parkinson’s disease. Nevertheless, many other diseases today are good indications for DBS like dystonia, essential tremor and Giles de la Tourette syndrome. Many papers say that DBS is like a “gold standard” in patients affected by dystonia or Parkinson's disease when pharmacological intake alone doesn't work or has lots of troublesome collateral effects. Since 2010, we started to use a stereotactical frameless technique. We noticed a real improvement in patients in terms of comfort, tolerability and reduced pain during surgery. At the same time, we obtained a very good precision in targeting, comparable to those of classical frame based surgery. Innovations, mostly in hardware such as leads, extentions and IPG, go on. We recently started to implant a new lead's generation named, “directional leads”. This lead has many different splitted contacts that allows the clinicians to steer the electrical field mostly wherever they want through the nervous tissue, obtaining clinical effect far from brain area, so as to avoid collateral effects. Since March 2016, we have performed 14 bilateral implantations for Parkinson’s disease and dystonia. At the time of reglage, when collateral effects like motor evoked unwanted responses or limbic effects have been elicited, switching the “hemi-contacts” allowed to make them disappear without any reduction in the desired beneficial effect. An issue we faced, was how to standardize all implanted patients, a shared rotational position of leads. As such, the clinicians can establish a number for any single contacts in order to compare results in different patients and in the single one over time as well. We also did not have an X-ray checking system in the Nexframe device, like basically any head-mounted and pin-fixed traditional stereotactical system has in itself. In other words, we needed a method that allowed to figure out the position of leads. We took two markers behind the ears to allineate during intraoperative X-ray checking. This brought to correct alignment of the lead's reference markers visible at the top of the whole group of contacts. In conclusion, even though the number of patients is low, we believe that directional leads bring to excellent results in terms of shaping of stimulation. They are a powerful tool in the hand of programmer clinicians, potentially able to improve the outcome of the patients. Splitting of contacts gives the chance to get a higher number of contacts allowing the clinician to choose among many stimulation's combination. Moreover, directional leads technology gives us the possibility to steer and deform the tridimensional electrical field shape. Warping and bending of electrical field, brings to a better results for patients, both lessening side effects and enhancing the positive benefits of stimulation. Our easy and reliable intraoperative tecnique is effective to correctly alineate in the same orientation the two leads of both sides.

  • WORKSHOP
Location: Athens
Speaker

Chair

Alain L Fymat

International Institute of Medicine and Science, USA

Speaker

Co-Chair

Jae Moon Lee

Kainos Medicine Inc., South Korea

Session Introduction

Selver Burcu TellioÄŸlu

Tarsus State Hospital , Turkey

Title: Clinical and neuropsychological study of natural course of light cognitive failure, alzheimer disease and parkinson dementia

Time : 14:10-15:10

Speaker
Biography:

Abstract:

Objective: 

The Objective of this study is to examine the natural courses of Alzheimer Disease (AD), Light Cognitive Failure (LCF) and Parkinson ‘s Dementia (PD) cases free of any therapeutic procedure and with neuropsychological test series; to determine the transformation ratio of these cases to dementia and to examine the courses of clinical factors. 

Tools and Method: 

120 patients consisting of 72 AD, 16 PD and 32 LCF patients and 24 healthy controls who are the spouses of the patients or healthy volunteers, who have applied to Mersin University Faculty of Medicine Education and Research Hospital Neurology Department between years 2007 and 2016, have been included in the research.

Patients have been invited to control visits once every 6 months and healthy individuals have been invited to control visits once a year.

Findings:

In the patient groups, functionality and DLA scores have considerably failed in comparison with the scores of control group. In the LCF group, MMSE, forward and backward counting range, calculation, abstraction, praxis, memory of word list, understanding, construction, clock drawing scores have been higher than the other groups but lower than the control group. In the LCF group, total NPI and NPI trouble scores have been lower than the other groups.  In the PDgroup, total NPI scores have been determined to be higher than the AD and LCF groups. Total NPI trouble score has been higher for the AD group when compared with PD and LCF groups. In the LCF group, for 11 % of the patients, diagnosis have transformed to AD in the control period. In the control visits, MMSE values of the control group have risensignificantly after the second visit. In the LCF group, falls in word list memory scores which are statistically meaningful have been determined in the first and third trials.

Result: 

In our study, we determined that 11,1% of the patients with LCF cogenesis had transformation to AD, in this group no transformation to PD has been observed in the control time, no transformation in the healthy control group has been observed.

 

Break: Networking & Refreshments 15:10-15:25 @ Europa Foyer
  • Epilepsy Therapeutics
Location: Athens
Speaker

Chair

Alain L Fymat

International Institute of Medicine and Science, USA

Speaker

Co-Chair

Jae Moon Lee

Kainos Medicine Inc., South Korea

Session Introduction

Rapita Naresh Sood

McGill University, Canada

Title: Role of the mTOR signaling pathway in epilepsy specifically in eIF4ebp2 KO mice

Time : 15:25-15:50

Speaker
Biography:

Rapita Naresh Sood has completed her PhD from University of Haifa Israel and presently doing her Postdoctoral studies from Goodman Cancer Research Center, McGill University in the laboratory of Dr. Nahum Sonenberg. She has published eight papers in reputed journals and has also received the Richard and Edith Strauss Fellowship which is a McGill Internal fellowship award for one year. Also, her project on epilepsy is giving a new direction to rescue the mTOR pathway which is a new perspective for future therapy of epilepsy.

Abstract:

Epilepsy, a common neurological disorder characterized by recurrent seizures that are unpredictable and sometimes progressively severe affecting 50 million people worldwide. Mutations in TSC1/2, PTEN and FMR1 genes cause Tuberous Sclerosis, PTEN hamartoma syndrome and fragile X syndrome respectively and lead to intellectual disability, autistic-like behaviour and epileptic seizures. Mutations in these genes cause upregulation of mTORC1 signalling, however the role of mTORC1 downstream effectors, such as 4E-BPs and S6K, in the pathophysiology of the disorders is not well understood. In the current project we set out to study the contribution of cap-dependent translation and 4E-BP2, downstream of mTORC1, in the susceptibility to seizures. Our previous study showed that deletion of 4E-BP2 leads to autism-like phenotypes and imbalance of excitatory to inhibitory synaptic activity. We recently found that eIF4ebp2 KO mice show reduced threshold to seizure-inducing agent (PTZ) at concentration of 70 mg/kg IP. As part of this project we would like to see whether inhibition of eIF4A would rescue or attenuate the seizure phenotype. The first experiment we are planning is to inject intraperitoneally WT and eIF4ebp2 KO mice with vehicle and eIF4A inhibitor. The experimental studies is still going on and furthermore, is needed to understand the role of mTOR signaling pathway in epileptogenesis, and that it may be a target for the development of novel therapies that eliminate the progressive effects of seizures.

Farnaz Nikbakht

Iran University of Medical Sciences, Iran

Title: Anticonvulsant and antiepileptogenic effects of metformin

Time : 15:50-16:15

Speaker
Biography:

Farnaz Nikbakht, before obtaining her PhD degree in Human Physiology from Shiraz University in 2007, she received an award from the Iran Ministry of Health and Education; she spent six months at Flinders University, Adelaide, Australia for completing her research on degenerative diseases. Now, as the Associate Professor of Department of Physiology, Iran University of Medical Sciences, she has managed several research programs and has conducted the thesis of several Masters and PhD students in her Lab. Since 2010 she has directed a research team on Epilepsy and Alzheimer’s diseases fields in her lab. Her research leads to publishing several articles.

Abstract:

Background: Current medications for epilepsy are just anticonvulsive agents and cannot protect against epileptogenic processes. On the other hand, theses anticonvulsive drugs are ineffective for one-third of epilepsy patients. Regarding these limitations, there is an urgent and growing need for a new drug to process both properties. Metformin, a common antidiabetic drug, has been shown to act as an anticonvulsive drug in some experimental models. However, the antiepileptic properties of metformin are not yet clear.

Materials & Methods: Sixty male Wistar rats are divided randomly into four groups: control, kainate (KA group), metformin+KA group and metformin group. Temporal lobe epilepsy was induced by intracerebroventricular (ICV) microinjection of 0.5 µg KA. Metformin was orally administered, starting two weeks before epilepsy induction. Following epilepsy induction, animals were monitored for behavioral seizure severity. Epileptogenesis was assessed by evaluating four factors: Hippocampal neuronal loss and neurodegeneration using Nissl and Fluoro Jade B(5 days after surgery); Neurogenesis using BrdU (5 days after surgery); Mossy Fiber sprouting, using Timm staining (30 days after surgery) and; EEG (30 days after surgery).

Results: Metformin as an anticonvulsant drug: the latency to seizure and the seizure severity were both reduced significantly, following metformin treatment (P<0.001). Metformin as antiepileptic drug: According to the Nissl and Fluoro-Jade B staining, the best protected areas in the hippocampus after metformin administration were CA3 and hilus (P<0.00). Behavioral EEG monitoring revealed that metformin-treated rats displayed spontaneous seizures at lower frequencies compared with epilepsy group. Metformin alone increased the neurogenesis which was even greater than Ka-induced neurogenesis. However, metformin-treated rats after epilepsy showed the immigration of new neurons to the hilar and CA3 areas. Metformin also reduced significantly mossy fiber sprouting.

Conclusion: Altogether we conclude that metformin acts not only as an anticonvulsant but an antiepileptogenic drug. 

 

Abraham Ratna Joseph Nayakanti

Avalon University School of Medicine, Curacao

Title: Anencephaly a chance of teratogenicity by Antiepileptic drugs during organogenic period

Time : 16:15-16:40

Speaker
Biography:

Abraham Ratna Joseph Nayakanti is an Assistant Professor in the Human Structure and Function Department, Avalon University School of Medicine, Curacao. He is a PhD Scholar in the Department of Anatomy in the Field of  Embryology of Renal Morphogenesis and Histogenesis, Faculty of Medicine at Vinayaka Missions University  and has completed his Master’s degree in Medical Anatomy at SVIMS University, India and has more than six years of teaching experience in various medical universities in India and abroad with presentations and publications in various international conferences and medical journals of anatomy and research. He has Successfully comleted Online course in Essential Skills in Medical Education, given by Association of Medical Education in Europe (AMEE) under Dundee University, Scotland.

Abstract:

Neural tube defects are very rare untill they are found in repeated deliveries. During routine collection of fetuses for the morphometrical and histological studies of renal developmental study, we found a rare anomaly with the defective closure of the cranial neuropore resulting in anencephaly. The case study consists of Intra uterine dead fetus with anencephaly which has spontaneously aborted. Service of Salem Polyclinic Hospital, in giving male aborted fetus for the study with the parent consent is appreciable. The diagnosis of suspected anencephaly was made on average at 21.3 weeks of gestation. The crown rump length was 14 cm and the crown heel length measurement of the fetus was 22 cm. In general there are various conginetal neural anomalies which appear to be similar to anencephaly.

Arindam Ghosh Mazumder

CSIR- Institute of Himalayan Bioresource Technology, India

Title: Exploring the anti-seizure potential of selective PI3K inhibitor in zebrafish model of pentylenetetrazole induced seizure

Time : 16:40-17:05

Speaker
Biography:

Arindam Ghosh Mazumder is a Senior Research Fellow, currently pursuing his PhD from CSIR-Institute of Himalayan Bioresource Technology, Palampur, Himachal Pradesh, India. He was awarded DST-INSPIRE Fellowship for pursuing PhD, sponsored by the Department of Science and Technology (DST), Government of India, 2013.

 

 

Abstract:

The role of mammalian target of rapamycin (mTOR), an evolutionary serine/threonine protein kinase, has been well documented in several disorders. In epilepsy research, mTOR pose as a very exhilarating target, as inhibition of its hyperactivation has been found to be effective in suppression of epilepsy and epileptogenesis. However the precise mechanism for the aberrant expression of mTOR, leading to the overexpression of its downstream genes, still remains blurred. Preclinical and clinical studies have revealed that decrease in PI3K/AKT/mTOR pathway hyperactivation have considerably reduced seizures. Hence, our study was designed to explore the anti-seizure potential of selective PI3K inhibitor (morpholine containing compound) on zebrafish model of pentylenetetrazole induced seizure. Zebrafish larvae of 7 days post fertilization were subjected to different concentrations of the selective PI3K inhibitor, following which they were exposed to pentylenetetrazole and recordings were scored on a 3 point scale. The best therapeutic concentration was selected and it was tested on adult zebrafish. Furthermore, fish brains were isolated and expressions of genes were studied in comparison to the epileptic fish. The results showed that the inhibitor distinctly reduced the seizure state in both larvae and adult fish in combination to decreasing the expression of various genes of the PI3K/AKT/mTOR pathway. These findings concluded that selective PI3K inhibitor has anti-seizure potential and can be explored in the near future as a potential antiepileptic.