Day2

  • Clinique SACCADE, Canada
  • Title:The Development of Consciousness in Autism
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Abstract:
Research on the neuronal and cognitive development of the human brain is increasingly making it possible to clarify the neural substrates associated with a variety of neurodevelopmental disorders such as autism. While such studies improve our understanding of the nature of these disorders, it nevertheless remains a challenge in autism research to understand the reasons for the heterogeneity of autistic profiles and how the varied characteristics of autism may be related to one another.
The Internal Structure of Autistic Thought hypothesis (referred to as the FISPA hypothesis, FISPA being the French acronym for Fonctionnement interne de la structure de pensée autistique) proposes that the condition of autism should fundamentally be considered a neurodevelopmental consciousness disorder. The early atypical connectivity of structural and functional brain networks known in autism could affect the development of functional and integrative neural systems that allow access to consciousness, namely the global neuronal workspace and the default network.
The FISPA hypothesis was developed from the experiential expertise of an autistic individual, Brigitte Harrisson, a social worker and autism specialist, and she and her team’s clinical observations of autistic individuals. Ms. Harrisson argues that developmental disturbances in the integrative neural systems could affect the ability to consciously process and integrate information about oneself and one’s environment from birth. An ensuing developmental cascade would then lead to a spectrum of alterations in the chronological stages of consciousness development, from body consciousness to environmental perception to self-awareness to the theory of mind, and finally, to meta-consciousness. According to the FISPA hypothesis, an autistic person may have to exert continuous cognitive effort as well as occasionally exhibit certain repetitive movements to engage the conscious processing of information.
Biography:
Dr. Catherine St-Charles Bernier is a doctor of neuropsychology (D. Psychology Laval University) and the director of clinical services at SACCADE, the Autism Center of Excellence™. Her experience with specialized and subspecialized psychiatric institutions both in Quebec and abroad (such as the CRA of Martinique) have enabled her to further develop her expertise in autism. Today, Dr. St-Charles Bernier oversees professionals in their application of the SACCADE™ model. In addition, Dr. St-Charles Bernier collaborates on the scientific component of the validation of the SACCADE™ model and interventions. She provides training and supervision to professionals in institutions throughout Quebec, France, and internationally. Dr. St-Charles Bernier taught at the Université du Québec à Rimouski (UQAR) for nearly a decade (2010-2020). She has contributed to various scientific articles (St-Charles Bernier et al., 2022; Mottron et al., 2007) as well as to projects in autism genetics

  • Clinique SACCADE, Canada
  • Title:The Development of Consciousness in Autism
  • Time :

Abstract:
Research on the neuronal and cognitive development of the human brain is increasingly making it possible to clarify the neural substrates associated with a variety of neurodevelopmental disorders such as autism. While such studies improve our understanding of the nature of these disorders, it nevertheless remains a challenge in autism research to understand the reasons for the heterogeneity of autistic profiles and how the varied characteristics of autism may be related to one another.
The Internal Structure of Autistic Thought hypothesis (referred to as the FISPA hypothesis, FISPA being the French acronym for Fonctionnement interne de la structure de pensée autistique) proposes that the condition of autism should fundamentally be considered a neurodevelopmental consciousness disorder. The early atypical connectivity of structural and functional brain networks known in autism could affect the development of functional and integrative neural systems that allow access to consciousness, namely the global neuronal workspace and the default network.
The FISPA hypothesis was developed from the experiential expertise of an autistic individual, Brigitte Harrisson, a social worker and autism specialist, and she and her team’s clinical observations of autistic individuals. Ms. Harrisson argues that developmental disturbances in the integrative neural systems could affect the ability to consciously process and integrate information about oneself and one’s environment from birth. An ensuing developmental cascade would then lead to a spectrum of alterations in the chronological stages of consciousness development, from body consciousness to environmental perception to self-awareness to the theory of mind, and finally, to meta-consciousness. According to the FISPA hypothesis, an autistic person may have to exert continuous cognitive effort as well as occasionally exhibit certain repetitive movements to engage the conscious processing of information.
Biography:
Isabelle Tremblay holds a master’s degree in psychology with a specialization in neuropsychology from the Université du Québec à Trois-Rivières (UQTR). Ms. Tremblay garnered her expertise in differential diagnoses for children, adolescents, and adults with autism from her years of experience working in rehabilitation centers, hospitals, and alongside child psychiatrists. As well as being a member of SACCADE’s team of instructors, she also coordinates research projects aimed at scientifically validating the SACCADE™ model. Ms. Tremblay was a contributor to the recent scientific paper “Autism as a neurodevelopmental consciousness disorder according to the Internal structure of autistic thought hypothesis (FISPA)” published by St-Charles Bernier et al. (2022).

  • Department of Bioinformatics,Germany
  • Title:A combined approach to discovering drug repurposing candidates targeting Alzheimer pathophysiology
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Abstract
Aims
The high number of failed pre-clinical and clinical studies for compounds targeting Alzheimer disease (AD) has demonstrated that there is a need to reassess existing strategies. Here, we pursue a holistic, mechanism-centric drug repurposing approach combining computational analytics and experimental screening data. The main objective of our joint approach is to suggest highly relevant drug repurposing candidates for testing in clinical trials in the context of AD.

Method
We combine drug-target information with knowledge graphs that represent essential pathophysiology mechanisms. The resulting Human Brain PHARMACOME (HBP) embeds all relevant drug-target interactions in the context of a massive collection of computable disease mechanisms underlying Alzheimer disease.

Results
To demonstrate its utility, we used the HBP to identify upstream controllers of posttranslational modification of the tau protein, with a strong focus on phosphorylated Tau (pTau), one of the hallmarks of Alzheimer’s Disease. Interestingly, HDAC6 was identified as one of the pleiotropic regulators controlling posttranslational modification of tau. In a dedicated drug repurposing (DR) approach, we established a HDAC6-tau assay and screened a repurposing library consisting of 5632 approved drugs for compounds that modulate Tau phosphorylation. We identified, profiled and validated 20 compounds that indeed modify pTau through HDAC6. Four compounds, and their known targets, were found to have a link to AD specific genes.

Conclusion
We identified new drug-target combinations and provided mechanistic explanations that help to improve our understanding of AD pathology and support future development of effective therapeutic strategies.

Biography
Dr. Vanessa Lage-Rupprecht a research scientist at Fraunhofer SCAI Bioinformatics. After her Diploma in Biology at the Rheinische Friedrich-Wilhelm-University in Bonn (Germany), she received her PhD in Experimental Neurophysiology at the University Hospital Bonn and continued her research in cellular neuroscience at McGovern Medical School (Houston, USA) and the University of Regensburg (Germany). At Fraunhofer SCAI Bioinformatics She work in the field of Applied Semantics and operate as a bridge builder between biomedical domains and informatics implementation strategies with focus on interoperability of data and knowledge.

  • USA Jersey Shore University Medical Center,USA
  • Title:Cytokine Storm Induced New Onset Depression In Patients With COVID-19. A New Look Into the Association Between Depression And Cytokines—Two Case Reports
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Abstract :
Background: Depression appears to be a common complication in patients during and post-COVID-19 infection. Understanding the mechanism of action of cytokines such as interleukin-6, interleukin10 and others in depression and in cytokine storm syndrome, the core component of COVID-19, could shine a new light on future treatment options for both disorders.
Objective: This review demonstrates the role of interleukins in COVID-19 pathogenesis and their role in depression.
Results: We describe cases we have treat3ed as an example for the dual role interleukins have in COVID-19 infection and depression and reviewed approximately 70 articles focusing on the role of interleukins in cytokine storm syndrome and depression
Conclusion: This review highlights the key features of cytokines in both diseases. As the scientific community has more time to recover and process the effect of the current pandemic, we believe that additional research will pave the way to diverse pathways to treat depression in these patients and others.

Biography :
Dr. Orna Alpert is a psychiatrist who specializes in Child and Adolescent Psychiatry and Psychosomatic Medicine. She treat children and adults with depression disorder, PTSD, delirium, somatization and drug and alcohol addiction. Her specialty involves the evaluation and treatment of patients with co-morbid medical illness and psychiatric symptoms. She have a special interest in organ transplantation and worked at the Children’s Hospital of Philadelphia and Yale-New Haven Hospital with liver, kidney and heart transplant candidates. During her time at the Medical College of Wisconsin, she was director of transplant services.As a result of the COVID-19 pandemic, She focused on patients who exhibited complications such as delirium, depression and Guillain-Barre Syndrome. Most of her work in recent years has focused on Consultation-Liaison Psychiatry or Psychosomatic Medicine. She remain active academically and continue to publish and give lectures.She recently received the honor of becoming a Fellow of the Academy of Consultation-Liaison Psychiatry.

  • Department of Cardiovascular & Metabolic Sciences,USA
  • Title:The role of gut microbes in altering susceptibility for the development of stroke
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Abstract:

Clinical studies report an association between the gut microbiota-derived metabolite trimethylamine-N-oxide (TMAO) and both risk of stroke and its adverse outcomes. However, experimental studies have yet to directly demonstrate a contribution of gut microbes to cerebral vascular diseases including stroke. In this presentation, we show that gut microbiota directly impact host susceptibility to stroke, and adverse outcomes following stroke, through the dietary choline, gut microbiota, TMAO pathway. In initial gnotobiotic mouse stroke model studies, fecal microbial transplantation into germ-free recipient mice from low versus high TMAO-producing human donors was shown to transmit capacity for TMAO generation and significantly impact stroke severity. Next, employing independent murine stroke models with conventional mice, we showed that dietary supplementation with either choline or TMAO enhanced both cerebral infarct size and post-stroke functional deficits. Finally, in additional gnotobiotic transplantation studies employing a synthetic microbial community lacking choline to trimethylamine (TMA) transforming activity ± genetically engineered human commensals (wild-type versus ΔcutC mutant), we show that harboring a functional gut microbial cutC gene is sufficient to transmit enhanced TMA(O) production, exacerbate cerebral infarct size and functional deficits within a host. Collectively, these studies reveal that gut microbiota in general, and the TMAO pathway specifically, directly impacts host susceptibility for stroke and its adverse functional outcomes.

  • Cairo University, Egypt.
  • Title:A DPP-1 Inhibitor Ameliorates Neurodegeneration in Aluminium Chloride Induced Alzheimer’s Disease Rats via Acting on Klotho, AKT/ERK and JAK/STAT Signalling Pathways.
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Abstract:
Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders contributing the majority of dementia cases worldwide. The main pathologic hallmarks of AD are senile plaques (SP) and neurofibrillary tangles (NFT) in addition to several molecular factors like neuroinflammation and increased oxidative. Klotho is an antiaging protein expressed by hippocampal neurons and plays a strikingly antioxidant, anti-inflammatory role. Klotho deficiency has been associated with hippocampal neurodegeneration and memory deficits together with elevated oxidative stress. Gliptins have been shown to dampen neurodegeneration via modulating glucagon-like peptide (GLP)-1. This peptide, acting on GLP-1R in the brain, exerts central anti-inflammatory and antiapoptotic effects. We have previously reported the neuroprotective effects of vildagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor in two different models of dementia and cognitive decline induced by high fat high fructose alone or with aluminium chloride (AlCl3) administration via enhancing klotho expression and activating its downstream signaling pathways. In the present study, we investigated the favorable effects of vildagliptin in a rat model of AD induced by AlCl3 oral administration alone (100 mg/kg/day) for 60 days. Rats were orally treated with Vildagliptin (10 mg/kg) for 60 days along with AlCl3 administration. Vildagliptin treatment enhanced general activities together with spatial memory and learning in open field test and morris water maze (MWM) test respectively. A significant increase of both hippocampal klotho expression along with an increase in its downstream effectors AKT and ERK phosphorylation with an inhibition of JAK2/STAT3 pathway were observed. These results were evidenced by an increase in hippocampal Bcl-2 expression and a decrease in hippocampal BAX expression which were subsequently accomplished with reduction in contents of inflammatory, apoptotic and oxidative stress biomarkers as TNF-α, caspase-3 and FOXO1. These findings confirm the neuroprotective role of vildagliptin is via enhancing Klotho protein expression together with activating AKT and ERK pathway and conversely inhibiting JAK/STAT pathway.

Biography:
Dr.Rasha Refaat Yossef
Part-Time assistant lecturer at pharmacology and toxicology department, Faculty of pharmacy, October 6 university, Giza, Egypt.
She did Master’s degree of Pharmaceutical Science, pharmacology and toxicology, faculty of pharmacy, Cairo university, Cairo, Egypt, 2020.Diploma of pharmacology and toxicology, faculty of pharmacy, Cairo university, Cairo, Egypt, 2009.
Bachelor of pharmaceutical science, faculty of pharmacy, Cairo University, Cairo, Egypt, 2006.

  • University of Concepción, Chile
  • Title:Covered-Stent Treatment of an Extracranial Internal Carotid Artery Pseudoaneurysm in a 3 Years-Old Child with 12-years Follow-up. Case Report.
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Abstract:
Introduction: Extracranial internal carotid artery (ICA) pseudoaneurysms in children, although uncommon, are life-threatening. Covered stents are a good alternative treatment, as they avoid the risk of open surgery and preserve the internal carotid artery. Long- term outcomes were unknown until recently. Report: In August 2008, a 3-years-old child was treated with a covered stent for a pseudoaneurysm in the extracranial ICA. A long-term follow up is presented. Results: The child was discharged with full recovery and without neurological sequelae. He has been followed-up and has remained asymptomatic for 12 years, with CTA- confirmed internal carotid artery patency, without deformation or evidence of significant re- stenosis. Conclusion: This the first report of the long-term outcome of a covered stent in a child treated at 3 years of age, with a 12-year follow-up. The good performance of the covered stent in this case reinforces its adoption as a first-line option in the treatment of extracranial ICA pseudoaneurysms in children.
Biography:
Dr. Roberto Sánchez, MD Professor of Surgery,Faculty of Medicine- University of Concepción- CHILE Fellow of the American College of Surgeons,Former Foreign Resident of Paris Hospitals,Foreign Associate Member Society of Vascular and Endovascular Surgery of French Language (SCVE),Non-European Membership European Society of Vascular and Endovascular Surgery (ESVS)

  • Southern Illinois University Carbondale, USA
  • Title:Frontal Volume as a Potential Source of the Comorbidity Between Attention-Deficit/Hyperactivity Disorder and Reading Disorders
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Abstract

Prefrontal volume reductions commonly are demonstrated in ADHD, but the literature examining prefrontal volume in reading disorders (RD) is scant despite their also having executive functioning (EF) deficits. Furthermore, only a few anatomical studies have examined the frontal lobes in comorbid RD/ADHD, even though they have EF deficits similar to RD and ADHD. Hence, we examined frontal gyri volume in children with RD, ADHD, RD/ADHD and controls, as well as their relationship to EF for gyri found to differ between groups. We found right inferior frontal (RIF) volume was smaller in ADHD, and smaller volume was related to worse behavioral regulation. Left superior frontal (LSF) volume was larger in RD than ADHD, and its size was negatively related to basic reading ability. Left middle frontal (LMF) volume was the largest in RD/ADHD overall. Further, its volume was not related to basic reading nor behavioral regulation but was related to worse attentional control, suggesting some specificity in EF relationships. When examining hypotheses on the etiology of RD/ADHD, RD/ADHD was commensurate to ADHD in RIF volume and both RD and ADHD in LSF volume (being midway between the groups), consistent with the multiple deficit/common deficit etiology hypothesis. Nevertheless, they also had an additional gyrus affected: LMF, consistent with the cognitive subtype hypothesis in its specificity to RD/ADHD. The few other frontal aMRI studies on RD/ADHD supported both hypotheses as well. For example, when we conducted a whole-brain VBM analysis on this data, we found clusters of reduced volume in the left precentral cortex in RD, various bilateral prefrontal regions in ADHD, and left medial and middle frontal gyri in RD/ADHD versus controls, along with other non-frontal regions. For all three clinical groups, clusters of smaller volume were found in the right superior frontal gyrus and striate (caudate) versus controls, being potential sources of shared etiology contributing to the RD/ADHD comorbidity. Given this, future research should continue to focus on frontal morphology in its endeavors to find neurobiological contributors to the comorbidity between RD and ADHD. Moreover, VBM and tracing were shown to be complementary, in that shared and dissimilar regions were demonstrated between the two methods, suggesting that both should continue to be used in research.

Biography
Dr. Kibby is a Full Professor in the Brain and Cognitive Sciences and Clinical Psychology programs within the School of Psychological and Behavioral Sciences at Southern Illinois University Carbondale. Her expertise include clinical child neuropsychology and developmental cognitive neuroscience. She studies shared and dissimilar contributors to neurodevelopmental disorders, especially reading disorders and ADHD.She and her lab have presented ~ 200 posters at national and international conferences, and she is a frequent invited speaker. She has 30 peer-reviewed publications as well as various book chapters. She also has received two grants from NIH that have supported her MRI work.

  • The Research Institute of Ophthalmology, Egypt
  • Title:Successful Oral Treatment of Third Cranial Nerve Palsy and Optc Neurits from Neglected Herpes Zoster in an Immunocompetent Patentt
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Abstract

Purpose: Herpes zoster (HZ) is an acute viral erupton caused by the reactvaton of varicella zoster virus (VZV), a herpes virus causing chicken pox in children. We aimed to report a 3- month neglected case of acute herpes zoster-induced third nerve palsy and optc neurits, followed by a late-onset keratouveits in an immunocompetent young adult.
Observations: A 36-year old immunocompetent Egyptan male patent presented with 3- month complaints of blurred vision and drooping of his lef upper eyelid that appeared 4 days after a herpetc rash. He had been diagnosed with herpes zoster ophthalmicus (HZO) of the lef eye. However, he had not received any systemic antviral treatment. The patent had an abnormal head posture with post-eruptve scars on the lef forehead and the nose tp. Examinaton revealed weakness of elevation and adducton, partal ptosis, and mid-dilated non-reactve pupil in the lef eye. A relatve afferent pupillary defect (RAPD) was present in the affected eye. His blood sugar and blood pressure were within normal limits. Contrast magnetc resonance imaging (MRI) showed no space-occupying lesion. However, there were
enhancement and enlargement of the lef optc nerve on T1-weighted images, denotng optc neurits. A diagnosis of acute lef third nerve palsy with pupil involvement and optc neurits secondary to HZO was made. Despite late treatment with oral acyclovir and prednisolone, the patent recovered. One and a half months later, he developed a late-onset
keratouveits about 8 months afer the rash onset. Afer the resoluton of the episode, oral acyclovir was contnued at a prophylactc dose (444 mg BID).
Conclusions aod importance: HZ is a rare cause of third nerve palsy with pupil involvement and optic neurits. Oral acyclovir and steroids were effective in the delayed treatment in this case. Abnormal optc nerve enhancement on MRI 3 months afer the appearance of vesicular rash may suggest chronic HZ activity. Concurrent optic neurits and third cranial nerve palsy in the absence of other signs of orbital apex syndrome can be seen in cases of HZO. Regular follow-up of patents with HZ is important for detectng recurrence and initatng prompt treatment.

Biography

Dr. Samah Ahmed Osman.She is a Consultant in Ophthalmology. She had obtained her Bachelor degree in Medicine and Surgery from the faculty of Medicine of Alexandria University in Egypt. She worked in French hospitals as a resident in Emergency & Surgery departments for one and half year. She returned home and she had obtained a Master degree in General Surgery from the faculty of Medicine of Cairo University. As she was always passionate about Ophthalmology, she made a ‘career shif’, and she had obtained a diploma in Ophthalmology from the faculty of Medicine of El Azhar University, as a second specialty. She believe in contnual learning and practcing in Medicine. Therefore, she joined The Egyptan Fellowship training program in Ophthalmology for 4 years. She had practced in specialized ophthalmology insttutes in several subspecialty departments. She had obtained The Fellowship of The Egyptan Board of Ophthalmology [FEBO]. She also succeeded in the examinatons of part 2 of The Fellowship of The Royal College of Physicians and Surgeons (FRCS) of Glasgow. She intend to take the examinatons of part 3 FRCS (Glasgow) next year.She took many visitor posts in The Research Insttute of Ophthalmology in Strabismus, Oculoplastcs, and Vitreo-Retnal departments. She is honored to have her frst publicaton (this case report) in The Americao Jouroal of Ophthalmology Case Reports. She work in a private clinic.

  • Institute of Biotechnology, Czechia.
  • Title:Requirements for SOX2 in Early Neurosensory Development
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Abstract

SOX2 is essential for maintaining neurosensory stem cell properties and it is involved in the early neurosensory development, in particular the brain and various sensory organs. SOX2 acts by maintaining an undifferentiated pro-neurosensory cell state that allows for proliferation in various developmental systems. SOX2 plays multiple roles in neuronal, sensory, and non-sensory development. At present, it is unclear how SOX2 achieves all these different functions. Interactions of SOX2 with other transcription factors likely represent a potential mechanism allowing for different roles of SOX2 in development. Several transcription factors have been shown to cooperate with SOX2 in different cell lineages, including C-MYC, Pax6, EYA1, SIX1, and CHD7. Additionally, the involvement of SOX2 in the early neurosensory development of cranial placodes remains unclear. To address this, we conditionally deleted Sox2 during eye, ear, and olfactory placode development. Early deletion of Sox2 eradicates all olfactory placode development, and disrupts retinal development and invagination of the lens placode. In contrast to the lens and olfactory placodes, the ear placode invaginates and delaminates NEUROD1 positive neurons. Furthermore, we show that SOX2 is not necessary for early ear neurogenesis, since the early inner ear ganglion is formed with near normal central projections to the hindbrain and peripheral projections to the undifferentiated sensory epithelia of the inner ear.

Biography

Dr. Gabriela Pavlinkova received her Ph.D. in Immunology in 2000 from Charles University, Prague, Czechia. After a postdoctoral training at University of Nebraska Medical Center, USA, she was appointed Assistant Professor at University of Nebraska Medical Center, USA in 2005. Since 2008, she is Head of Laboratory of Molecular Pathogenetics, Institute of Biotechnology Czech Academy of Sciences, Prague, Czechia.

Research interest

My main research interest is to understand molecular aspects of neuronal development. I am focused on genetic mutations affecting transcriptional regulation during embryonic development, the molecular mechanisms of developmental programming, and identification of the molecular causes of abnormal embryonic development and disease predispositions.