8^th Global Summit on
Neuroscience and Neuroimmunology

Biography:

Vicente Felipo is Director of the Laboratory of Neurobiology and of the Program on Neuroinflammation and Neurological Impairment of the Centro de Investigacion Principe Felipe in Valencia (Spain). He has 30 years of experience in research on the mechanisms, diagnosis and treatment of neurological alterations in hyperammonemia, hepatic encephalopathy and by exposure to food and environmental contaminants. He has published more than 300 manuscripts, 3 patents, edited 7 books, organized more than 20 International Symposia and directed more than 26 doctoral theses. He has been first Secretary of International Society for Hepatic Encephalopathy and member of different national and International Committees.

Abstract:

Several million patients with liver cirrhosis suffer minimal hepatic encephalopathy (MHE), with psychomotor slowing and mild cognitive and coordination impairments that increase accidents, falls and hospitalizations and reduce their quality of life and life span. MHE is an important clinical, social and economic problem (1).

Hyperammonemia and peripheral inflammation act synergistically to induce these neurological alterations. We have identified some alterations of the immune system associated with appearance of the neurological alterations in cirrhotic patients: increased activation of all subtypes of CD4+ T-lymphocytes and of its differentiation to Th follicular and Th22 (2).

Patients died in HE show neuroinflammation in cerebellum, with activation of microglia and astrocytes and loss of Purkinje cells (3).

We study in animal models the mechanisms by which inflammation leads to neuroinflammation; how neuroinflammation alters neurotransmission and how this leads to cognitive and motor alterations. We identify therapeutic targets and assess whether treatments acting on these targets improve cognitive and motor function in rats with MHE.

Rats with MHE show neuroinflammation in hippocampus, with microglia and astrocytes activation and increased IL-1b and TNFa. This is associated with altered membrane expression of NMDA and AMPA receptors which, in turn, impairs spatial learning and memory. Rats with MHE also show neuroinflammation in cerebellum, associated with altered GABA transporters and extracellular GABA which impair motor coordination and learning in a Y maze.

These alterations may be reversed by treatments that a) reduce peripheral inflammation: anti-TNFa (4,5), reduce neuroinflammation: sulforaphane (6,7); increase extracellular cGMP (8,9).

The mechanisms by which inflammation induces neuroinflammation, how this impairs neurotransmission and leads to cognitive and motor alteration would have common components in different pathologies including chronic diseases associated with inflammation, ageing and some mental and neurodegenerative diseases. Treatments useful to improve these mechanisms in MHE may be also useful in these pathologies.

Biography:

Prof. Nevzat Tarhan became a Psychiatrist in GATA in 1982. He became a professor of psychiatry in 1996. In 1998, he became the representative of Turkey in Memory Center of America. As Tarhan closely observes the social life due to being a psychiatrist, he makes an accurate analysis of the social life and touches on the importance of "Community Psychology" in every media platform.

Prof. Nevzat Tarhan has always targeted investment in people and used his material-spiritual resources towards this direction. He expresses through his actions that he will continue the same objectives until the end of his life, under his approach of the faith. Currently, he is the Founder and Rector of the Üsküdar University and carries out the NPÄ°STANBUL Brain Hospital Chairman of the Board of Directors, which is Turkey's first neuropsychiatry hospital. He has more than 100 publications, of which 31 are international. He speaks English and German.

Abstract:

Anti-NMDA receptor encephalitis was firstly described in 2007. Up-to this date more than 400 cases have been described, making the syndrome rather unrare. It is an autoimmune disorder where the NMDA receptors are targeted. The disease may affect anyone at any age and any gender. The patients usually have a viral-like prodrome of lethargy, upper respiratory symptoms, headache, nausea, fever…etc. The presenting symptoms of the syndrome are mainly psychiatric. The patients manifest various psychotic symptoms like delusions, disorganized thoughts and behaviours, paranoid ideation, hallucinations, mood lability and cognitive deterioration. After 1-3 weeks of neuropsychiatric symptoms, the patient suffers from neurological complications such as global alterations in consciousness, catatonic-like states, dysautonomia and seizures. The patients may need to be hospitalized for 3-4 months. Agressive treatment with corticosteroids and immunotherapy is needed. Most patients respond to this treatment. However, they may have significant cognitive and behavioral abnormalities like deficits in executive functions, impulsivity, behavioral disinhibition, and sleep disturbances that need further follow-up. Psychiatric and neurological symptoms are treated with psychotropic drugs as in other neuropsychiatric syndromes. Some patients may need neurorehabilitation. The diagnosis requires cerebrospinal fluid (CSF) work-up. In CSF lymphocytic pleocytosis, elevated protein and oligoclonal bands are found. Demonstrating antibodies against NMDA receptors in CSF and/or serum gives a solid diagnosis of the disease. Cranial magnetic resonance imaging (MRI) may be normal in half of the cases. Electroencephalography (EEG) is usually abnormal with slowed and disorganized activity.

Biography:

Dr. Barış Önen Ünsalver is currently an Assistant Professor of Psychiatry at the Uskudar University, Istanbul, Turkey. She has been working at the NP Istanbul Brain Hospital for 9 years. She has been working in the area of neuropsychiatry, neuropsychophilosophy, and published over 40 papers in peer-reviewed journals, as well as invited chapters in books. Her research and clinical interests focus on psychosomatics, neurophilosophy and brain-stimulation therapies in neuropsychiatric disorders.

Abstract:

Various studies have indicated that inflammation might have a significant role for the development of psychiatric disorders such as depression, anxiety, alcohol use disorder, schizophrenia, autistic spectrum disorders and neurodegenerative disorders like Alzheimer’s disease. The evidence that has accumulated over the years suggests that there exists a cross-talk between the neurotransmitters and the immune system. This cross-talk might have a role in the etiology of psychiatric disorders.  Inflammation may affect different neurotransmitter systems. For example, inflammation may increase the expression and function of serotonin transporter and GABA receptors in the hippocampus, or induces the enzyme indoleamine 2,3-dioxygenase, which may eventually influence glutamatergic neurotransmission. Immune cells are also adept at synthesizing and releasing neurotransmitters like GABA. GABA exposure inhibits the inflammatory response in vitro and in vivo, in a mouse model of obesity. This cross-talk can influence the response to anti-depressant drugs. In fact, one mechanism in the therapeutic effects of antidepressants might be their anti-inflammatory effects. Inflammatory response markers like IL-6, TNF-alpha, and CRP in plasma decrease over time in patients that respond to treatment. The suggested sources of inflammation in psychiatric diseases are psychological stress, early life stress, obesity, inflammatory diet (high-fat diet, imbalance of n-6/n-3 polyunsaturated fatty acids), oxidative stress due to ethanol metabolism, insufficient sleep and unbalanced gut microbiota. In this session cases of neuroinflammation in chronic psychiatric disorders will be presented with a brief review of current literature on the subject.

Biography:

Dr. Alper Evrensel is currently an Assistant Professor of Psychiatry at the Uskudar University, Istanbul, Turkey. He has been working at the NP Istanbul Brain Hospital for 10 years. He has been working in the area of neuropsychiatry, neuropsychophilosophy, and published over 50 papers in peer-reviewed journals, as well as 4 invited chapters in books. His research and clinical interests focus on gut-brain axis and fecal microbiota transplantation in neuropsychiatric disorders.

Abstract:

Contrary to the general belief, a fetus is not sterile. Gut microbiota becomes colonized to the fetus in the intrauterine period. Microorganisms play a very significant role in the development of the immune system and the brain of the fetus. There is a bidirectional symbiotic relationship between gut microbiota and the body. This interaction is determinant on human health. Gut microbiota has fundamental effects on neuro-developmental processes such as blood-brain barrier formation, myelination and neurogenesis. There is a relationship between dysbiosis of microbiota and neuropsychological disorders, particularly depression. Colonization of pathogen bacteria in the gut and their metabolites (endotoxins) lead to immune response. Microorganisms affect the brain via the immune system, neuroendocrine system and nervus vagus. Nutrition, stress and medication lead to dysbiosis by changing the microbiota composition. It is also possible to purposefully manipulate the gut microbiota. Dysbiosis may be restored by changing gut bacteria composition with probiotics and fecal microbiota transplantation (FMT). Probiotic bacteria have a potential to be used in depression treatment. FMT may be a sign of hope in treatment-resistant chronic psychiatric disorders in the future. The door to the mysterious world of gut-brain relationship seems to have just been opened.

Biography:

Abstract:

The central nervous system has historically been considered immune-privileged; however this privileged position mostly consists of adaptive immune responses with restricted access of  infiltrating lymphocytes into the brain parenchyma, while cells of the innate immune system — microglia — are abundant in the brain. Microglia is also considered a key player in many neuroinflammatory conditions. Microglial cells respond to infectious agents such as LPS with reactive phenotype and changes in expression of certain markers such as Iba1. Reactive microglia are also found in the brain during neuroinflammatory processes in  depression, bipolar disorder, post-traumatic stress disorder (PTSD). We used animal model of PTSD in order to test how chronic stress affects the neurogenesis, reactivity of microglial cells as well as their density in the dentate gyrus of the hippocampus and whether hippocampal volume is changing during PTSD. According to our results, 10 days after stress onset the number of Iba1+ microglial cells in the dentate gyrus of the hippocampus increased substantially compared to the control group (Mann–Whitney, p=0,028). However we did not see any inflammatory foci, i.e. microglial nodules. The intensity of Iba1+ staining of as well as the size and shape of cells did not differ from the control group. The hippocampal volume did not change significantly. We propose that neurotoxic or neuroprotective role of microglia cells can change depending on the microenvironment, such as in presence of certain cytokines, interleukins, hormones that lead to corresponding changes in the molecular profiles of glial cells. The particular mechanisms of microglia activation and its role in neurogenesis is discussed.

Biography:

Dr. Jameelah Saeedi is a certified Saudi Neurologist who specializes in Multiple Sclerosis and Neuroimmunological Diseases. She received her medical qualification from King Abdulaziz University in Saudi Arabia in 2001 followed by two-boards in Neurology from Saudi Commission for Health Specialties and the Jordanian Medical Council in 2007. Dr. Saeedi is alumni of University of British Columbia where she pursued her fellowship and training in Neuroimmunology and Multiple Sclerosis with Prof. Peter Rieckman in 2009. In 2010 she received two more fellowships in Electromyography and Boutlinum Toxin Injection treatment from the University of Toronto .She is one of few leading pioneers who holds vast knowledge, experience, sub-specializes and practices Multiple Sclerosis and Neuroimmunological Diseases in Saudi Arabia. She has been working at King Fahad Medical City as a Subspecialty Consultant and KFMC Comprehensive Neuroimmunology Program Director .She is currently working at King Abdullah Bin Abdulaziz university hospital in Saudi Arabia

Abstract:

Neuromyeltis optica (NMO) is an immune-mediated inflammatory disease of the central nervous system (CNS). It typically affects the optic nerves and spinal cord, causing recurrent, severe optic neuritis and/or transverse myelitis. NMO was initially described as a variant of multiple sclerosis (MS). However, it is currently considered a separate disease entity that shares some clinical and radiological features with MS. Some reports have suggested that NMO was misdiagnosed as MS in 30%–40% of cases, especially before aquaporin (AQP)-4 testing was available. In 2004, NMO-IgG was first reported to be associated with the disease, and its antigenic target is the most abundant CNS water channel termed AQP-4. Since this discovery, the disease spectrum has significantly widened, and some patients are being diagnosed with the disease even without manifesting the typical involvement of the optic nerve and spinal cord. Multiple diagnostic criteria have evolved over the years, and in 2015, new diagnostic criteria were published, wherein a unified term, NMO spectrum disorder with either positive or negative AQP-4 antibodies, has been used. Although approximately 80% of NMO patients are positive for serum AQP-4 antibodies, some can exhibit negative results despite using the most sensitive available technique. In this negative group of patients, a new antibody targeting myelin oligodendrocyte glycoprotein (MOG)—a protein expressed in myelin and on the surface of oligodendrocytes in the CNS—has been described. During my presentation, I will go over the new diagnostic criteria for NMO, the radiological features of the disease, the differences between anti-MOG NMO and anti–AQP-4 NMO, as well as some practical points in the diagnosis and management of the disease. I will also present real cases that I have encountered during my practice.

Biography:

Dr. Denis Bouboulis offers over 20 years of experience and expertise as a nationally and internationally recognized practitioner in this field. A board certified physician licensed in Connecticut, New York and Pennsylvania in the area of Allergy & Immunology and Internal Medicine. Experience in private practice and hospital settings, and in the development of treatment and testing devices. Internationally recognized as a leading expert on the autoimmune disorder PANDAS.

Abstract:

To present illustrative patients with infection-induced autoimmune encephalopathy (IIAE) who manifest symptoms and signs of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) and are successfully treated with an anti-infective and immune modulatory protocol. Methods: Six children age 5 to 17 years with the diagnosis of IIAE associated with various infections and comorbid conditions including humoral immunodeficiency and Autism Spectrum Disorder (ASD) are described. Pertinent literature from 1958 to the present is reviewed. Antimicrobial and high dose (1 gram per kilogram total body weight) intravenous immune globulin (IVIg) therapy was administered every 8 weeks according to an established anti-infective and immune modulatory protocol. Informed consent by the parents and legal authorization was obtained in all cases. Neuroradiological testing was not performed in any of the cases. Results: The combination of antimicrobial medication followed by IVIg in this cohort was well-tolerated leading to improvement in symptoms and signs of IIAE allowing tapering or discontinuation of maintenance medications. Conclusion: IVIg is a safe and beneficial therapy in IIAE, PANDAS and ASD impacting favorably on underlying humoral immune deficiency and infectious-induced CNS autoimmunity in this small and highly selected cohort. The present findings are awaiting further replication by other investigators and should be further explored relative to the optimal dose and duration of therapy.

Biography:

Ahmed Ali Hussein completed a master's degree at the age of 26 years in microbiology and immunology from the University of Qadisiyah - College of Science had gotten a master's degree in 2016. It has been published of a number of research's in local and international journals, I have a book about immunology title " Medical Immunology ".  I was assigned to supervise a number of undergraduate graduate studies for the purpose of obtaining a diploma degree, and I also provided a lot of advice to postgraduate students (Masters and PhD) in the field of immunology.

Abstract:

There are several sites in the body that do not develop immune responses to pathogens, tumor cells, or histoincompatible tissue transplants, these sites, include the brain, eye, testis, ovary, and placenta, so-called because of mechanisms of immune tolerance that operate to protect the tissues from immune-mediated damage. The central nervous system complying the brain and spinal cord is an essential organ for survival, because the inflammation in these sites can lead to loss of organ function. The blood-brain barrier plays an important role in maintaining the separation of CNS from the systemic immune system but the presence of the blood-brain barrier, does not, on its own, provide immune privilege. Activated immune cells secret molecules that are neurotoxic and the encasement of the brain in the skull does not permit excessive infiltration of immune cells. Neurons are highly susceptible to damage by inflammatory responses and have limited ability to regenerate. Since the brain lacks a lymphatic system, and the immunoregulatory mechanisms in the brain circumvent damage to neurons and supporting cells such as oligodendrocytes and astrocytes. Mechanisms known to operate in the protection of neurons from attack by CD8 + cytotoxic T cells involve lack of expression of HLA class Ia A, B and C receptors by neurons. Astrocytes express cell surface FasL which promotes apoptosis in activated T cells by engagement with Fas. (Figure 1). Another mechanisms known to operate in the protection of neurons from attack by natural killer cells is the induced expression of HLA class Ib G receptors that bind to NK inhibitory receptors such as KIR. Astrocytes upregulate surface PD-L1 receptors which promotes apoptosis in activated T cells by engagement of PD-1 receptors. In addition, microglial cells inhibit T cell proliferation by mediating depletion of tryptophan with IDO (indolamine 2,3-dioxygenase).

Biography:

Abstract:

Medicine is a field in science that concerns itself to the improvement of an organism’s well-being by having a catena to the field of Healthcare. It is a branch of science which treats diseases and unriddles illnesses which have no available cure like autoimmune diseases, like Lupus. Lupus or Systemic Lupus Erythematosus (SLE) is a disease where the immune system attacks the body’s own cells mistaking it for a foreign aggregate of a person’s body that usually targets the female population. Due to this, many researches of this disease have focused mainly on female Lupus cases, leaving the affected male population with little knowledge about their case and about themselves. As part of the research enterprise, an introspection among the physical, mental, emotional and social aspects of a male lupus patient was done to promulgate information about the accordant aspects of a person’s self and to see any effects of the disease to the manliness of a male Lupus patient. The research was conducted through In-depth interviews and email interviews of one male lupus patient, having open-ended questions as its cornerstone being a case study. Results of the research were accomplished by sense-making, which furthered the knowledge of male lupus patients being physically deduced, mentally polished, emotionally reliant to God and family, socially selective and still relevantly male.

Biography:

Dr. Elmaleh is an Associate Professor at Harvard Medical School and the Director of Contrast Media Chemistry at the Massachusetts General Hospital. He is a renowned molecular imaging expert and inventor of numerous molecular imaging agents including three drugs that are in use in man or in late stage clinical trials, including the radiopharmaceutical preparation of (2FDG) which has been used in millions of PET imaging procedures. Dr. Elmaleh also recently received patent protection for the use of 18F-FDG PET for imaging atherosclerosis, for tracking inflammation within plaques, and for monitoring the response to drug therapy; a promising use that should be part of the future diagnostic armament. Dr. Elmaleh is a founder of several biotech companies including Molecular Insight (formerly Biostream) and Mersana (formerly NanoPharma) that recently closed a drug deals for over $700 million with big pharma. He also co-founded Puretech health that recently went public on The London Stock Exchange, at a valuation over $500 million. Dr. Elmaleh holds a BS in Physics and Chemistry, and an MS and PhD in Organic Chemistry. Dr. Elmaleh is a recipient of numerous NIH and DOE grants. His recent work includes extensive research on imaging compounds, platforms to improve the speed and effectiveness of cardiovascular disease diagnosis, ischemia, infarction, and plaque formation which have enabled several drug technologies licensed from MGH to a new start-up. He is a co-author on over 130 publications and book chapters, an inventor of over 100 issued and pending patents in a range of disciplines, including molecular imaging and pharmaceuticals.

Abstract:

Alzheimer’s disease is a significant unmet medical need. It is the sixth leading cause of death in the United States, affecting one in eight elderly Americans and nearly 35 million adults worldwide. Globally, it is estimated that more than $800 billion is spent annually caring for dementia patients. The disease has no cure or viable commercial or clinical treatment option, and patients continue to rely on inadequate therapies to treat symptoms. FDA-approved drugs for the treatment of Alzheimer’s disease, such as AriceptTM (donepezil) and NamendaTM (memantine), temporarily treat symptoms of dementia without impacting disease progression. Analysts have projected that disease-modifying Alzheimer’s therapeutics will be rapidly adopted as a breakthrough product. ALZT-OP1 is a novel, patented combination of two small molecule drugs (OP1a and OP1b) previously approved by the United States Food and Drug Administration (FDA) for non-CNS indications. Our combination use of these molecules is proprietary, as is our formulation, preparation, low dosing and delivery administration that increases brain accessibility, all of which sets us apart from prior uses. The previously approved dosing and delivery of these molecules is ineffective for AD treatment due to its limited blood concentration availability. Our in-vitro, in-vivo APP/PS1 and Tg2576 animal models results support ALZT-OP1’s mechanism of action and utility, demonstrating that our drug attacks and modifies the complex neurodegeneration process associated with aging. Two separate (Phase , Ib) human blood and CSF pharmacokinetic studies in a mix of 48 normal and AD subjects confirm the blood and brain drug combination availability in healthy and AD patients. These studies indicate ALZT-OP1 has the potential to halt Alzheimer’s disease early in a safe administration and allowed for the Phase III,  SPA FDA agreement.

Biography:

Umur Kayabasi is a graduate of Istanbul Medical Faculty. After working as a resident in Ophthalmology, he completed his clinical fellowship program of Neuroophthalmology and electrophysiology at Michigan State University in 1995. After working as a consultant neuro- ophthalmologist in Istanbul, he worked at Wills Eye Hospital for 3 months as an observer. He has been working at World Eye Hospital since 2000. He has chapters in different neuro- ophthalmology books, arranged international symposiums, attended TV programs to advertise the neuro- ophthalmology subspecialty. He has also given lectures at local and international meetings, plus published papers in neuro-ophthalmology. He became an assistant professor at Uskudar University- Istanbul in 2015.

Abstract:

Background: Recent research suggests that Tau is the culprit lesion along with neuroinflammation in the etiology of Alzheimer' s Disease ( AD ).  Retina is the extention of the brain and is the most easily approachable part of the central nervous system.  Detection of the pathological protein accumulations may be possible by using spectral domain optical coherescent tomography ( SD-OCT ) and fundus autofluorescein ( FAF ).  There is evidence showing that retinal plaques start accumulating even earlier than the ones in the brain.  Most recent Tau protein images in the brain consist of normal or reverse C-shaped paired hellical filaments.

 Methods: 20 patients with PET proven AD were examined by SD-OCT and FAF.  Mean age was 72. Hypo or hyperfluorescent retinal  lesions were scanned by SD-OCT and C shaped paired hellical filaments were investigated in a masked fashion.  The researchers agreed on the shape of the lesions. Both C-shaped ( normal or reverse ) filaments and thinner  fibrillary structures were taken into consideration.

 Results: In all the patients, paired hellical filaments that exactly corresponded with the histopathologic and cryo-EM images of Tau in terms of shape and dimension were detected along with thin fibrils and lesions similar to amyloid beta.  The number of the retinal filaments  and other abnormal proteins was in concordance with the severity of the disease process. The advanced retinal filaments had normal or reverse paired C shapes and thin fibrils had the shape of histopathologic images seen in early developmental stages of the disease.

 Conclusions: Retinal images of Tau were disclosed for the first time in live AD patients.  Retinal neuroimaging is a trustable biomarker and tool for monitoring the disease.

Biography:

Anastasia-Ervina Sela is a student at the 4th year of Nursing at the Technological Educational Institute of Athens.

Abstract:

Dementia is one of the most serious complications of Traumatic Brain Injury. This disease can be mainly caused by road accidents and falls, clearly because the effect of the force on the brain is stronger and the changes in brain function are more radical. A retrospective cohort study, which was approved by the University of California, San Francisco and Human Research Committee and was performed from January 1, 2005, through December 31, 2011 (follow-up, 5-7 years), found that among 51799 patients with trauma, 4361 developed dementia compared with 6610 patients with non-TBI trauma. The correlation of Traumatic Brain Injury and Dementia is evident especially in the larger age groups of the population. In addition, several epidemiological studies suggest that Traumatic Brain Injury (TBI) is a risk factor for Dementia, particularly for Alzheimer’s Disease (AD), although a significant association has not always been detected. There is evidence that in mild and severe Traumatic Brain Injuries most patients have emerged after years Dementia in contrast to those patients who just had a minor injury. In conclusion, Traumatic Brain Injury can be associated to a significant degree with the risk of developing Dementia especially to the people with increased risk. Given the high rates of TBI to the general population serious Dementia prevention measures should be taken in such incidents and clearly to carry out more studies and even longer in order to fully understand the mechanisms that affect between traumatic brain injury and dementia.

Biography:

Dr. Taguchi obtained her B.Sc. from Tokyo University of Agriculture, in Tokyo, Japan and her Ph.D. from Osaka University Graduate School of Medicine, in Osaka, Japan. She worked as a postdoctoral research fellow and a research associate in Dr. Morris White’s lab at Harvard Medical School, Boston, USA. Dr. Taguchi is interested in the interaction between lifestyle-related diseases such as diabetes and neurological disorder such as dementia. Her lab currently studies on the molecular mechanism of diabetes-associated cognitive decline. She is particularly interested in the roles of neural insulin/IGF1R signaling in cognitive functions and the effects of existing medications on brain functions (drug repositioning ). Dr. Taguchi has received several grants from Grant-in-Aid for Scientific Research on Innovative Areas, Grant-in-Aid for Scientific Research, Grant-in-Aid for challenging Exploratory Research, and private foundations in Japan.

Abstract:

The aging systemic milieu leads to a decline in hippocampal neurogenesis and cognitive functions, which also occurs in diabetes. Despite growing concern regarding the potential role of diabetic drugs in neural abnormalities, their effects on progressive deterioration of neurogenesis and cognitive functions remain unknown. Metformin, a biguanide antidiabetic medication is the first-line drug for type 2 diabetes and lowers blood glucose levels by decreasing basal hepatic glucose output and increasing glucose uptake by skeletal muscle through activation of the AMP-activated protein kinase (AMPK). Here we show that prolonged treatment with metformin enhances hippocampal neurogenesis while countering the microglial activation in the context of the combination of aging and diabetes in mice. Although chronic therapy with metformin fails to achieve recovery from hyperglycemia, a key feature of diabetes, it improves hippocampal-dependent spatial memory functions accompanied by increased serine /threonine phosphorylation of AMPK , atypical protein kinase C ζ(aPKC ζ ), and Insulin Receptor Substrate 1 (IRS1) , a major mediator of the insulin/IGF1R signaling,  in the hippocampus. Our findings suggest that signaling networks acting through long-term metformin-stimulated phosphorylation of AMPK, aPKC ζ/λ, and IRS1 serine sites contribute to neuroprotective effects on hippocampal neurogenesis and cognitive function independent of a hypoglycemic effect.

Biography:

Pierre A. MORGON is CEO of MRGN Advisors and Regional Partner for Switzerland at Mérieux Développement. Pierre is also Chairman of the Board of Virometix, as well as Non-Executive Director to the Boards of Theradiag, of Eurocine Vaccines and of Vaccitech. Pierre has over 30 years of experience in the global life science industry, especially with vaccines and immunotherapy, at the helm of international operations, in C-level positions at global level and as CEO of start-ups. He is a lecturer in several MBA programs in world-class business schools and in life science conferences, as well as to the Mass Challenge biotechnology incubator in Switzerland. He holds a Doctorate of Pharmacy, a Master in Business Law and a MBA. He is also an alumnus of INSEAD and IMD.

Abstract:

The vaccine segment is anticipated to be one of the fastest growing one of the healthcare industry and several leading firms have stepped up vaccine investments in recent years. Unlike therapeutic agents, vaccines are administered to healthy individuals only once or very infrequently during a life time. Vaccines generate well-documented positive externalities, yet their poor awareness and acceptability among vaccine end-users may contribute to resurgence of transmissible diseases and consequently trigger governmental interventions such as mandating vaccination. In addition to technical and clinical development per the highest quality standards, bringing new vaccines to market requires carefully orchestrated programs targeting the multiple types of stakeholders along the entire value chain and addressing their respective purchasing behavioral drivers. Against a backdrop of anti-vaccination buzz and vaccine fatigue, successful global launch and sustainable usage of a vaccine requires the development of a multi-pronged strategy addressing  all aspects in relation to acceptability (e.g. the motivation to immunize despite the quasi-disappearance of the disease), accessibility (e.g. supply chain services), availability (e.g. mechanisms ensuring reliability of supply) and affordability (e.g. tiered pricing policy taking country differences in per capita income into account). Leveraging novel technological advances can positively influence the ability to activate these levers successfully.