12^th World Congress on Dementia and Alzheimer Rehabilitation April 11-12, 2019
Hotel Park Inn by Radison Stockholm Hammarby Sjostad, Sweden

Biography:

Junyang Wang graduated from Wenzhou Medical University in 2015 and he is currently a MD student majoring in Neurology at Zhejiang University School of Medicine, P.R. China. His research interests focus on exploring the novel bio markers for AD patients using multi modality MRI.

Abstract:

Background/Aims: To use cerebral blood flow (CBF) measurements with the arterial spin labeling (ASL) technique to assess difference between ApoEε4 gene carriers and noncarriers and to observe the regulating effect of CBF on memory functions.

Methods：A total of 62 healthy elderly subjects without subjective memory impairment and with normal score of Mini–Mental State Examination (MMSE) were drawn from the Alzheimer’s disease Neuroimaging Initiative (ADNI) database; of whom 23 were ApoEε4 gene carriers and 39 were no carriers. The following three Regions of Interest (ROI) were selected for CBF measurements: medial temporal lobe (hippocampus, Para hippocampal gyrus and uncus), inferior parietal lobe (supramarginal gyrus，inferior parietal lobule and angular gyrus), and frontal cortex (anterior cingulate gyrus, middle frontal gyrus and medial frontal gyrus). At the same time, the Rey Auditory Verbal Learning Test (RAVLT) was performed on all subjects to test their verbal memory function, and the results were correlated with the CBF.

Results: The CBF in the ROIs was positively correlated with verbal memory function in the non-carriers. By contrast, in ApoEε4 carriers the CBF value from the ROIs was negatively correlated to verbal memory function.

Conclusion: For ApoEε4 carriers, an increased CBF does not compensate for memory function loss. That is to say, the regulating effect of CBF is affected in ApoEε4 carriers.

Biography:

Bao Wangxiao graduated from China Medical University in 2014, and she is currently a PhD student majoring in Neurology at Zhejiang University School of Medicine, P.R. China. Her research interests focus on exploring the novel biomarkers for TBI patients using quantitative proteomics and integrative bioinformatics method. She has published 8 papers in journals of related areas.

Abstract:

Background/Aims: Traumatic brain injury (TBI) initiates a complex pathological cascade of secondary insults following the initial mechanical injury. The present study was aimed at identifying the potential key genes, pathways and possible mechanisms in parietal and temporal cortex after mild-to-moderate TBI.

Methods: The array data of GSE104687 were downloaded from the Gene Expression Omnibus (GEO) database, including 98 postmortem cortex tissues from donors experienced mild-to-moderate TBI and 91 samples from donors without TBI. We performed Gene Ontology annotation, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses and constructed a protein-protein interaction (PPI) network for the identified differential expression genes (DEG).

Results: 33 DEGs with a ± 2-fold change (p < 0.01) were obtained between TBI goups and non-TBI groups, including 7 upregulated and 26 downregulated genes. The altered genes were enriched in cytosol, translational initiation and structural constituent of ribosome. The protein-protein interaction (PPI) network consists of 14 nodes and 63 edges. 9 genes (RPL41, RPS4X, RPS7, RPL17, RPL27, RPL23, RPS15A, RPL24, RPL7A) were identified as the hub genes with the most significant meaning.

Conclusion: We have demonstrated a global view of the altered genes, interactions, and their related pathways in traumatically injuried cortex using bioinformatics methods. The present paper helps contribute to a more detailed understanding of the long-term pathophysiologic process after TBI, which might be transformed into clinical practice.

Biography:

Ms. Apeksha Shrivastava is pursuing her Ph.D. degree in pharmaceutical chemistry from Jamia Hamdard (NIRF rank:2), she has done her B.Pharm & M.Pharm from Bhupal Nobles College of Pharmacy Udaipur, Rajasthan, India. Before joining Ph.D. she served as an Assistant Professor for two years at Nandini Nagar College of Pharmacy, Nawabganj, Gonda. She is currently working of drug design discovery of Anti-alzheimers agents.

Abstract:

The research on peptidomimetic inhibitors of Prolyl Oligopeptidase for various disorders viz. Alzheimer’s, Schizophrenia, Inflammation, Parkinson’s, Depression, etc. is being carried out since more than three decades, but still no drug have made it through the clinical trials, possibly because of poor pharmacokinetics. This might have engrained from the fact that all the structures submitted to the clinical trials were having similar chemical structures. Our study aimed at identifying novel small molecule non peptidomimetic inhibitor for prolyl oligopeptidase enzyme that could serve as starting point for developing newer drugs for inhibition of the enzyme. A structure based virtual screening of MDPI database was conducted on of prolyl Oligopeptidase enzyme (3DDU PDB ID), the identified hits were subjected to computational ADME screening, thereafter, MM/GBSA studies were performed to check the stability of the ligand-receptor complex. Nine hits were then subjected to prolyl oligopeptidase inhibitory assay in triplicates, among which one compound MM4 displayed good inhibitory potential of 100 µM. Furthermore, MD simulations of MM4 and reference was carried out to study the overall stability of lead-receptor complex and also to identify important interactions that were not apparent from docking study. Hence, discovery of novel small molecule non peptidomimetic prolyl Oligopeptidase inhibitor was accomplished.

Biography:

Benjamin has completed his bachelor of medical science (honours class I) at the age of 22 in Professor Glernda Halliday’s laboratory at the brain and mind centre, University of Sydney. He is currently working as a research assistant to finalise his honours thesis into a publication and is planning to start his PhD in exploring the cognitive symptoms of Parkinson’s Disease starting 2019.

Abstract:

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, characterised by motor symptoms in sufferers. There is a well-established link between motor symptoms and the reduced supply of the neurotransmitter dopamine (DA) due to the loss of midbrain dopaminergic (DA-) neurons alongside increased Lewy pathology. PD patients may also develop non-symptoms with dementia highly prevalent in individuals (~80% of PD sufferers). PDD is not explained by a sole deficit in the neurotransmitter dopamine and the pathology changes associated with non-motor symptoms remain elusive in PD. Emerging evidence suggests that another neurotransmitter, noradrenaline (NA) which the locus coeruleus (LC) is a chief supplier in human brains, may be affected in PDD.

The aim of this study is to examine the severity of LC pathology in PDD, PD and healthy age-matched controls. Immunohistochemistry with antibodies against tyrosine hydroxylase (NA-neuronal marker), alpha-synucleinopathy and phosphor-tau was applied in the rostrocaudal planes of the LC using post-mortem human brain tissue. We hypothesize that specific regional and cell type degeneration in the LC will be more severe in PDD due to the projections from these LC regions to prefrontal cortex and hippocampus. Our study has confirmed that the pathological deterioration of the LC in PD compared to controls is obvious, revealed by; reduced NA-neuronal number and increased α-synuclein deposition. We further reveal significant differences between PD and PDD with even greater amounts of α-synuclein pathology and a more substantial reduction in the number of NA-neurons at caudal levels of the LC in PDD.

Biography:

Ellie Robinson-Carter is an illustrator, researcher, creative dementia practitioner and lecturer based in Falmouth, UK. Ellie devises creative frameworks and invites individuals to take ownership of them, fostering their authorial voices and personal narratives. Working locally, nationally and internationally Ellie works with people living with dementia and their carers, using creative practice to nurture individual’s self-confidence, independence and self-expression. She also collaborates with other creative practitioners such as illustrator Violeta Noy and poet Sally Crabtree.

Abstract:

Biography:

Nowadays due to economical and social progress the average age of world’s population has been increased, what results in increasing number of diseases related with old age. These diseases are dementia and Alzheimer’s disease.

Alzheimer’s disease is a chronic neurodegenerative disease that usually starts slowly and gradually worsens over time. Affected people increasingly rely on others for assistance. In developing countries it is a great challenge to take appropriate care of affected people and handle with the social, psychological, physical, and economic pressures, which places a burden on patients and their caregivers.

Abstract:

Lali Esebua is the 4th year medical student of  Tbilisi State Medical University.  She is taking the 8th semester in Lublin Medical University, within the framework of Erasmus programme. She has 2 publications : “The reasons of delayed medical assessment in oncology patients”, “The pain syndrome and sleep disorders in paliative care”, which are published in local university magazine.

Biography:

Robert J. Hedaya, MD, ABPN, CFM, DLFAPA  is board certified in psychiatry and psychopharmacology, and pioneered functional medicine in the neuro-psychiatric field. as clinical professor of psychiatry at Georgetown University medical center, he teaches courses including psycho-neuro-immuno-endocrinolgy. He is a faculty member at the institute for functional medicine, author of three books, and the founder of the national center for whole psychiatry. Dr. Hedaya is an editorial volunteer for advances in mind-body medicine and alternative therapies in health and medicine, has been featured in national media, and is a nationally and internationally recognized speaker.

Abstract:

It is widely recognized that the current treatment approach to subjective and mild cognitive impairment (SCI, MCI) and early dementia offers little in the way of efficacious treatment. Decades of research based on various linear models (e.g., amyloid, acetylcholine) with targeted pharmaceutical treatments have failed to produce clinically meaningful results. On the other hand, basic science and systems biology have identified and elucidated multiple modifiable (and mutually interacting) pathophysiological systems which increase vulnerability to neurodegenerative disorders such as SCI, MCI and various dementias. The majority cases of dementia are not unitary in etiology, but rather involve disturbances of multiple systems and are thus pathophysiologically impure. Even such APOE4 homozygotes generally have multiple contributing pathophysiologies, the etiological imprecision of our diagnostic terminology and continued use of a linear medical paradigm results in dismissal of relevant and modifiable pathophysiological contributors to dementia. Hence, diagnostic imprecision must be replaced with etiological precision. Underlying pathophysiological processes which are involved in cognitive decline include: central insulin resistance, mitochondrial and oxidative dysfunction, loss of trophic (nutrient, hormonal, immune, enrichment) support, immune dysfunction and infection, toxicity, cardio-vascular dysfunction, trauma, structure and lifestyle. The clear association between these pathophysiologies, their clinically measurable biometric parameters, and cognitive decline provides a clear treatment map, which is being used to reverse SCI, MCI and early to mid-stage dementia. A large trial of the functional medicine method is currently funded. This presentation will review the evidence and a series of cases demonstrating stabilization and recovery of cognitive function in these disorders.

Biography:

Dr. Dheeraj Chaudhary is a consultant forensic psychiatrist. He has a CCT in forensic psychiatry. He is a member of the Royal College of Psychiatrists MRC Psych, United Kingdom. He has a post graduate diploma PGDip in psychiatry from the Univeristy of Manchester, UK. He has a medical degree in Medicine and surgery. He is also approved by the secretary of the state, United Kiungson, under Section 12 (2) of the Mental Health Act 1983 (amended 2007) as having specific expertise in the diagnosis and treatment of mental disorders.

Abstract:

There is little research evidence reviewing depression in psychotic disorders. The symptoms can range from mild moodiness to severe depression and suicidal behaviours. It can be a diagnostic challenge in delineating depression from negative symptoms in psychotic disorders. Equally in clinical practice the treatment can be particularly problematic.

This presentation will look at the current understanding of the psychopathology, diagnostic concepts and treatment methodologies of depression in psychiatric disorders.

Biography:

Dr. Chandni Nigam is a graduate of Imperial College London, UK and is an ophthalmologist by profession. She has also completed a BSc in surgery & anaesthesia from her alma mater. She has held the position of president of the Imperial College Ophthalmology Society and is a published author of peer-reviewed articles.

Abstract:

The anaesthetic state and natural sleep share many neurobiological features and yet are two distinct states. The hallmarks of general anaesthesia include hypnosis, analgesia, akinesia, and anxiolysis. These are the principal parameters by which the anaesthetic state differs from natural sleep. These properties are mediated by systemic administration of a combination of agents producing balanced anaesthesia. The exact nature of anaesthetic narcosis is dose dependent and agent specific. It exhibits a relative lack of nociceptive response and active suppression of motor and autonomic reflexes. Surgical anaesthesia displays a signature EEG pattern of burst suppression that differs from REM sleep, representing more widespread disruption of thalamo-cortical connectivity, impairing information integration and processing. These differences underpin successful anaesthetic action. The following is a comprehensive discussion of the differences between natural sleep and anaesthetic induced unconsciousness as induced by balanced anaesthesia.

Biography:

Dr. Surena Vahabi is an associate professor in School of Dentistry, Shahid Behesti University of Medical Sciences, Iran. His reserach interests are dentistry, biogene marker etc. 

Abstract:

Background: Epilepsy is a major concern in both developed and under developing countries and one of the oral manifestations of Epilepsy is gingival overgrowth. Since the cellular mechanisms behind the gingival overgrowth has remained unknown especially in pediatrics, the aim of this study was to investigate the effect of CSA and PHT on the bio gene marker expression and compare it among adults and pediatrics.

Methods: Gingival fibroblasts which had been harvested from adults and pediatrics with normal gingiva were incubated with CSA and PHT, and then cultured for 48 hours. MMP (1 , 2), TIMP, Col , Eln, Lysyl, Cat L, B and mRNA level in culture were determined by reverse transcription polymerase chain reaction (RT-PCR), amount of  TGF_B and EGF were assessed by enzyme-linked immunosorbent assay(ELISA). The alpha error level was set at 0.05 for statistical significance.

Results: CSA and PHT stimulated the TGF_B and CAT_B productions and inhibited expression of MMP1 by fibroblasts. CSA suppressed TIMP in pediatrics but PHT stimulated its expression. In adults, both CSA and PHT increased TGF_B, Lysyl and EGF level. CSA reduced Eln level whereas PHT stimulated its level. PHT increased the CAT B level when CSA inhibited TIMP expression

Discussion: It seems that in pediatrics MMP1/TIMP system and in adults Lysyl/Eln pathway play an important role in impaired collagen metabolism.

Biography:

She is an associate professor of neurology in Aristotle University, Greece. In 1996, she got title of specialized neurologist and in 2013, elected as a permanent member of the University Ast. professor(AUTh), Greece. She has published more than 90 papers in reputed journals and has been serving as an editorial board member in more than 20 journals.

Abstract:

Copper is associated with the endogenous PrPC and PrPSc contributing to the pathogenesis of spongiform encephalopathy (CJD). A 44-year-old male with a history of inherited wilson's disease (hepatolenticular degeneration), mild liver injury for 12 years and bipolar psychosis during the last months, was admitted in our department due to speech and cognitive disturbances. Upon his admission, he had motor aphasia and psychomotor retardation without any other neurological signs and with Glasgow Coma Scale score 13/15. Laboratory examination including liver enzymes, copper and serum ammonia was normal. The brain MRI showed increased T2 signal in the caudate nuclei attributed to copper deposition in the context of Wilson's disease. In the electroencephalogram, periodic sharp discharges were found initially unilateral and then generalized.

His clinical condition was deteriorated rapidly presenting mutismus, myoclonic jerks, deterioration of consciousness, and within a few days the patient presented myoclonic status epilepticus without response to benzodiazepines or other antiepileptic treatment. He passed away a few days later.

The clinical picture, the positive 14-3-3 protein in the CSF and the new brain MRI that demonstrated elevated DWI signal not only in basal ganglia but also in brain cortex (cortical ribbon sign) made the diagnosis of CJD possible. The detection of PrP^Sc in CSF using the RT-QuIC method, which has 99.4 -100% specificity for CJD, made the diagnosis of CJD definite. This is the first reference to the Wilson and Creutzfeld-Jakob disease co-morbidity in case literature, which suggests the possible association of copper with the pathogenesis of CJD.

Biography:

Chithapuram Satheesh has completed his PhD at the age of 25 years from Andhra University and postdoctoral studies from Stanford University School of medicine. He is the director of a premier bio-soft service organization. He has published more than 25 papers in reputed journals and has been serving as an editorial board member of repute.

Abstract:

Encyclopedia of bioanalytical methods for bioavailability and bioequivalence studies of pharmaceuticals (E-BABE): It is a unique encyclopedia involving bioanalytical methods for bioavailability and bioequivalence (BA/BE) studies of pharmaceuticals for suitable method selection with thousands of combinations and searches against these methods. Most scrutinized literature was collected from different sources including pubmed. This database has been curetted using published methods for all most all pharmaceuticals. Required information for regular method development/validation such as IUPAC name, structure, solubility, chromatographic conditions, instrumentation information like HPLC, LCMS detection parameters, sample preparations, recovery details, limit of detection and limit of quantification, Tmax, Cmax etc., for routine application in BA/BE studies of pharmaceuticals was incorporated including official pharmacopeias information such as European Pharmacopeia, Japan Pharmacopeia and US Pharmacopeia. Database includes drug based bioanalytical methods covering most required fields and external database links of important drug portals such as drug bank, Rxlist, MEDLINE plus, KEGG Drug ID, KEGG Compound ID, Merck manual, pubchem compound ID, pubchem substance ID and USFDA. Searching/querying the database is through drug name, chemical formula or structural search by smiles format. Keen selections of bioanalytical methods for pharmaceutical analysis or regular quality control are also possible with E-BABE. E-BABE was built understanding the needs of pharmaceutical industry and laboratories including cros working on BA/BE studies. Presently it has nearly of 5,000 methods and it will be updated regularly. 

Biography:

Michelle Regina L. Castillo has completed her MD at the age of 27 years from the University of the Philippines college of medicine. She is a 2nd year radiology resident at the Philippine General Hospital, the country’s largest tertiary hospital. She has received a leadership award during her medical school

Abstract:

Hemichorea-hemiballismus is a rare presentation of nonketotic hyperglycemia, usually involving elderly females. A 71-year old female, with poorly controlled diabetes, presented with a one-month history of involuntary unilateral movement beginning with the left arm spreading to the ipsilateral lower extremity. Computed tomography (CT) imaging of the brain revealed nonspecific hyperdensity in the right basal ganglia. Further work-up with the use of Magnetic Resonance Imaging (MRI) was done showing abnormal signals in the right basal ganglia. In this case, we note the significance of detecting rare findings in diabetic patients through different imaging modalities such as CT and MRI, as differentiated from other more common pathologies causing neurologic symptoms. Prompt diagnosis would alert the clinician to the cause of the movement disorder. Correcting the hyperglycemia reverses this condition. 

Biography:

Jong Moon Kim is a MD in department of rehabilitation medicine in CHA Bundang medical center, CHA University School of Medicine. He is associated with rehabilitation and regeneration research center in CHA University, South Korea.

Abstract:

Introduction:

Previous studies of repetitive trans cranial magnetic stimulation (rTMS) has been shown possibility of efficacy to relieve cognitive dysfunction from Alzheimer dementia. However, because the rTMS protocols used in each study are different, there are no objective data that reveal most effective protocol. And frequency of the stimulation is still on debate in protocols of rTMS. Therefore, we conducted an experiment to determine more effective stimulation between high and low frequencies in cognitive function improvement when rTMS was applied in Alzheimer-induced mouse model.

Methods:

Thirty-six mice were included in this research and those were divided into three groups: control group with no experiment, control group with saline injection in cerebral ventricle and Alzheimer-induced mouse group with amyloid beta injection in the ventricle. Each group was divided into high frequency rTMS, low frequency rTMS, and no treatment subgroups. The rTMS treated groups were stimulated for 2 weeks, 5 days a week (Figure 1). High frequency rTMS group received rTMS with 20 Hz, 2s, 40 trains, 28s interstimulus interval, with total 1,600 pulses; and low frequency rTMS group received rTMS of continuous 1 Hz and 1,600 pulses in total. Both rTMS applied to the whole brain of the mouse and the intensity was 1.26 tesla. Y Maze test and novel object recognition task (NORT) were used for assessment of cognitive function and measured before rTMS and 1^st and 2^nd week after the rTMS.

Results:

Before rTMS, the Alzheimer-induced mouse group showed lower Y maze and NORT scores than the other control groups, and there was no difference among the subgroups in each group. After initiation of rTMS, Alzheimer-induced mouse group showed increments of spontaneous alteration in Y Maze and recognition of novel objects in NORT in both high and low frequencies of rTMS compared to non-stimulated subgroup at 1^st and 2^nd week (Figure 2, 3). There were no statistical differences in scores of Y Maze and NORT between high and low frequency at 1^st and 2^nd week after the rTMS.

Conclusions:

Both high and low frequency rTMS in Alzheimer-induced mouse brought improvement of cognitive function, which may be used as a therapeutic method to treat Alzheimer’s disease. Studies on the pathophysiology of rTMS effect and long term follow up are needed.

Biography:

Ms Kaliopi Dimitrakoudis studied medicine from University of Toronto, 1996 in department of neurology. He did is post-graduation from University of Ottawa, May 2002, and then did clinical fellowship from the same University. At present working in St Joseph's Health Centre, Toronto. He is a RCPSC Specialist in Neurology.

Abstract:

Years of medical research have confirmed the validity of Attention Deficit Hyperactive Disorder (ADHD) as a neurobiological disorder of the central nervous system. However, ADHD has been misunderstood from the beginning. For many years both physicians and lay persons questioned the existence of ADHD. More recently, rather than deny its existence outright, ADHD is challenged more indirectly by having its importance trivialized. This popular trivialization of ADHD is my topic. The trivialization of ADHD takes many forms: in claims that ADHD is seriously over-diagnosed, that its treatment is a stimulant medication rather than a prescription, and that what people see as ADHD is just the effects of new cultural developments weakening our capacity to stay focused. It points to traits accentuated with new digital technologies that present information in an emotionally satisfying but limited way. Similarly dismissive is the myth that ADHD is a condition that affects everyone in the population. (Aren’t we all just a little ADHD?). Other popular tropes are that ADHD is a social construct (in some de-legitimizing sense of that term), the product of bad parenting, or the result of living in the modern world. In this paper, I challenge the trivialization of ADHD on three grounds. First, I discuss how ADHD involves the dysregulation of neurotransmitter systems. This section will discuss ADHD from a molecular biology standpoint, focusing on neurotransmitters, drug targets, and neuroanatomy. Second, I argue that the popular myths of ADHD are not supported by the most current neuroscience into the disorder. This then leads into the third and final point I want to make: the recent trivialization of ADHD can have tragic consequences for those with the disorder: namely, they create stigma and are a form of epistemic injustice. I draw on lived experience accounts to show how the myths of ADHD lead to harmful consequences for those with the disorder. Recognition of the reality of ADHD patients as unique is a necessary pre-requisite to promote the well-being of those with ADHD.

Biography:

Ms Kaliopi Dimitrakoudis studied medicine from University of Toronto, 1996 in department of neurology. He did is post-graduation from University of Ottawa, May 2002, and then did clinical fellowship from the same University. At present working in St Joseph's Health Centre, Toronto. He is a RCPSC Specialist in Neurology.

Current Status: Active Member as of 01 Jul 1996

CPSO Registration Class: Independent Practice as of 27 Jun 2002

Abstract:

Years of medical research have confirmed the validity of Attention Deficit Hyperactive Disorder (ADHD) as a neurobiological disorder of the central nervous system. However, ADHD has been misunderstood from the beginning. For many years both physicians and lay persons questioned the existence of ADHD. More recently, rather than deny its existence outright, ADHD is challenged more indirectly by having its importance trivialized. This popular trivialization of ADHD is my topic. The trivialization of ADHD takes many forms: in claims that ADHD is seriously over-diagnosed, that its treatment is a stimulant medication rather than a prescription, and that what people see as ADHD is just the effects of new cultural developments weakening our capacity to stay focused. It points to traits accentuated with new digital technologies that present information in an emotionally satisfying but limited way. Similarly dismissive is the myth that ADHD is a condition that affects everyone in the population. (Aren’t we all just a little ADHD?). Other popular tropes are that ADHD is a social construct (in some de-legitimizing sense of that term), the product of bad parenting, or the result of living in the modern world. In this paper, I challenge the trivialization of ADHD on three grounds. First, I discuss how ADHD involves the dysregulation of neurotransmitter systems. This section will discuss ADHD from a molecular biology standpoint, focusing on neurotransmitters, drug targets, and neuroanatomy. Second, I argue that the popular myths of ADHD are not supported by the most current neuroscience into the disorder. This then leads into the third and final point I want to make: the recent trivialization of ADHD can have tragic consequences for those with the disorder: namely, they create stigma and are a form of epistemic injustice. I draw on lived experience accounts to show how the myths of ADHD lead to harmful consequences for those with the disorder. Recognition of the reality of ADHD patients as unique is a necessary pre-requisite to promote the well-being of those with ADHD.

Biography:

Shima Ebrahimikhonacha is PhD student in neuroscience research center, faculty of medicine, Shahid Beheshti Medical Sciences University. She passed her MSc corses in Semnan University of medical sciences and worked on “Investigation of the role of central beta adrenergic receptors in the enhancing effect of voluntary exercise on learning and memory in rats”. The results of this research have been published in behavioral brain research in 2010 (208:189–193). She did some expriments in Pasteur institute of Iran about Alzheimer Desease and Shahid Beheshti Medical Sciences University in epilepsy and chemical kindlig. These investigations have resulted in 2 publication  papers in reputed journals and 3 in national journals.
 

Abstract:

It has been shown that brain glucose metabolism impairment, obesity and diabetes could lead to cognitive decline and Alzheimer’s disease (AD) pathogenesis. Kisspeptin (KP) a G-protein coupled receptor neuropeptide has been suggested as a link between energy balance and reproduction. Some studies have shown that attenuation of KP signaling decreases metabolism and energy expenditure. KP is detected in the hippocampus and causes promotion of excitatory synaptic responses through modulation of postsynaptic signaling. The purpose of this study was to investigate the possible protective role of kisspeptin on cognitive function in rat model of AD using Morris Water Maze (MWM) task. Reference spatial learning and memory and reverse spatial learning and memory have been measured in this study. Rats were injected bilaterally by Aβ1-42 (MWM) or saline as vehicle into the hippocampal CA1. One week later, Kisspeptin13 (0.75 or 1 µg/µl) or saline as vehicle were injected intra cerebroventricularly before each training session for 3 days. The results of our investigation showed Aβ could not disrupt reference spatial learning but impaired significantly spatial reference memory, by increasing escape latency and decreasing time spent in the target zone. This impairment was reduced by KP in both doses. In another part of this study spatial reverse learning and memory was performed by changing the platform position. Aβ injection impaired both reverse learning and memory in MWM task. The Learning and memory deficits were significantly reversed by KP injections.

In Conclusion, it seems that KP as a neuropeptide could be a candidate for improving memory deficits resulting from Aβ toxicity in which needs to be further investigated.

Biography:

Shuba Hahta-id has graduated MTCS with a 3.49 GPA Class of 2008 and then went to Massage Therapy School in 2009. He is graduated in 2009 with a 4.0 GPA and then granted employment at a 4 Star Spa answering 345/350 questions right on the National Certification Exam and an Oath of Initiation, to do only good and to mend, taking away pain mentally, physically and emotionally. Now, 10 years later, he is providing for sure approach eliminating aspects of mental phenomena. Also, he initiated removal of corrupt Sheriff in 2015 beginning endeavor of transitioning the Prison for Profit System in America.

Abstract:

The direct correlation of sound, wording, attached with intention has a direct effect on neural networking where even proofs shown through experiments, over seen by Moran Cerf, provide ability to affect motor function precisely by projecting sound to certain areas of the brain to influence decision. This can be similarly applied through conscious affirmations which are also directly related to what is experienced in what we perceive to be reality. Certain phrasing in wording and even certain words alone have a great effect on what becomes programmed into an individual’s neural transmission carried out in systematic behaviors which have been previously defined under terms which brought about this conference. Furthermore as it’s proven each person having their own bio electromagnetic field sending and receiving transmission of data and this gains further insight into the mental phenomena of anxiety when an individual is unaware of the mechanics of their being, as all emotional frequencies are picked up by the signaling in one’s brain, granted the proofs we are all composed of light to begin with and sound is simply vibrations of light encoded with information. This also explains depression bipolar and other mental phenomena which I explain in other speeches to be granted presentation at future events hosted across the globe granted sponsorship. The direct focus on rephrasing mental disorder to mental phenomena also correlates to future experiences under causality of reality where the merge of psychology and physics provide key insights into a new direction for neurology research providing proofs in betterment of human treatment and understanding.

Biography:

Sophie Dechene is a Consultant Child and Adolescent Psychiatrist in private practice in her own centre, Ottignies-Louvain-La-Neuve, Belgium (May 2016- Feb 2018). She has good knowledge in IT (Windows and MAC).

Abstract:

Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) is a serious medical condition in childhood belonging to the PANS (pediatric acute-onset neuropsychiatric syndrome) category. Affected children are still frequently misdiagnosed as suffering from a psychiatric illness of psychosocial origin and their health can be affected for many years if left either untreated or treated only with psychotropic medication. Clinical symptoms typically have a waxing and waning course. This syndrome can present with OCD (obsessive compulsive disorder) symptoms, tics, restricted food intake and various other neuropsychiatric pathologies, such as different forms of anxiety, depression and sometimes isolated neuropsychiatric symptoms including increased urinary frequency, bed-wetting and sleep disturbance. The long-term risks are significant with not only severe psychological suffering, but also impaired stages of development in every area of life. Although PANDAS remains a diagnosis of exclusion, the important aetiological factor to look for is an infection with, or the asymptomatic presence of, Streptococcus A. A differential diagnosis must be made to distinguish PANDAS from other syndromes in the PANS spectrum without infectious triggers and PITANDS (pediatric infection-triggered autoimmune neuropsychiatric disorders) where non-streptococcal infections are implicated. Today, we give an overview of the current literature on PANDAS and present a clinical case of a boy suffering from PANDAS, who was first misdiagnosed as epilepsy and then with a psychiatric illness. The epilepsy was diagnosed during the first acute episode when the boy presented with a mild confessional state and, after excluding other aetiological factors, a degree of learning difficulty probably contributed to the diagnosis of a psychiatric illness. A 10 day-treatment with amoxycillin and ibuprofen given during the fourth acute episode led to a complete recovery. This case emphasizes the need to educate mental health professionals about the illness. Furthermore, given the elevated risks of false positive and false negative diagnoses and taking into consideration the pressure brought by distressed parents, professionals need to have a good awareness of this illness. Taking thorough personal and family histories combined with exhaustive mental, physical and neurological examinations is recommended to make a PANS diagnosis and the presence of or an illness related to Streptococcus, will direct you to a diagnosis of PANDAS. Other factors can contribute to a diagnosis of PANDAS, including the presence of autoimmune diseases such as rheumatic fever or streptococcal-mediated Sydenham chorea, recent travel in low income countries where the prevalence of Streptococcus in the general population is high or a recent generalized skin or throat infection.