International Conference on
Alzheimer's Disease & Associated Disorders

May 7-9, 2018 | Rome, Italy

Program Schedule

  • Keynote Speaker

    Time:

    Title

    Title: Early Prevention of Alzheimer’s Disease? Scientific Justification and Current Strategies

    Karen Ritchie
    University of Edinburgh, United Kingdom
    Biography
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    Biography

    Karen Ritchie
    University of Edinburgh, United Kingdom

    Prof Karen Ritchie is a neuropsychologist and epidemiologist, who began her career with the Health Services Evaluation Unit, University of Oxford (Sir Richard Doll) and the Social Psychiatry Research Unit, MRC Australia. She is currently Director of the French National Institute of Medical Research (INSERM), Research Unit 1061 (Neuropsychiatry) in Montpellier. The research work currently being undertaken by this group includes population, clinical and molecular studies of neurological and psychiatric disorders notably dementia, depression, post-traumatic stress disorder, suicide, sleep pathologies, and care evaluation. She has also acted as consultant to the Mental Health Division of the World Health Organization and is a member of the Board of the European Institute for Women's Health. She is currently also Visiting Professor, Centre for Clinical Brain Sciences, University of Edinburgh.



    Abstract
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    Abstract

    Karen Ritchie
    University of Edinburgh, United Kingdom

    Epidemiological studies suggest a complex interaction of risk and protective factors which contribute differentially to the probability and timing of Alzheimer’s disease (AD) onset. By modeling intervention scenarios it may be demonstrated that public health prevention strategies focusing on the most potent and potentially reversible risk factors could have a highly significant impact on disease incidence over the coming decade. This research has been validated across several countries and integrated into the recent Lancet report on the future of AD management. Exposure to these risk factors occur, however, primarily in middle age suggesting that strategies to prevent or delay disease onset should be carried out much earlier than is currently the case. Prevention programs carried out in the preclinical phase of AD will require the development of outcome measures able to detect brain changes in the absence of clinical signs. Recommendations for the design of preclinical prevention strategies are presented along with early results from the PREVENT-AD multi-site research project.

    Keynote Speaker

    Time:

    Title

    Title: Potential Gene, Drugs and Stem Cell Therapy at Critical Period in Alzheimer’s Disease Mice

    Yoo-Hun Suh
    Gachon University, Korea
    Biography
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    Biography

    Yoo-Hun Suh
    Gachon University, Korea

    Professor Yoo-Hun Suh is now Chaired Professor and President of the Neuroscience Research Institute of Gachon University. He was the founding president of Korea Brain Research Institute. He won Korea’s Most Distinguished Scientist Award, the National Government Medals and other many prizes. He was selected one of 20 outstanding Korean Medical Scientists and one of 21 outstanding Korean Scholars of the 21st Century. He is an editor and editorial board member for 6. He first cloned the gene for epinephrine synthesizing enzyme, PNMT and has greatly contributed to the discovery of a new potential gene and factors for AD, the development of potential stem cell and drugs for AD and PD.



    Abstract
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    Abstract

    Yoo-Hun Suh
    Gachon University, Korea

    Alzheimer’s disease (AD) is characterized by the accumulation of amyloid plaques and neurofibrillary tangles accompanied by cognitive dysfunction. To investigate the regulatory genes responsible for the neuropathology in AD, we performed microarray analysis in APPV717I-CT100 transgenic mice and isolated the S100a9 gene. These results clearly show that the upregulation of S100a9 gene plays an important role in the neuropathology and memory impairment in AD, suggesting that the regulation of this gene has a therapeutic potential for AD. We found that Dehydroevodiamine×HCI (DHED), Carboxy DHED, Minocycline BT11 and SF-6 had neuroprotective, memory or motor enhancing activities using various in vitro and in vivo models. DHED might be one of the potential therapeutic candidates for AD. We also examined whether intracerebrally or intravenously transplanted human adipose-derived stem cells (hASCs) could have therapeutic or preventive effects in AD/PD mice model. We demonstrated that intracerebral or intravenous injection of hASCs rescued memory deficit and gave benefits of blocking the pathogenesis in the brain of Tg mice by reducing the number of plaques and neuropathology. Hence, we demonstrated that hASCs are expected to be preventive and therapeutic approach for AD& PD. However, the optimal stage of the disease for stem cell transplantation to have a therapeutic effect has yet to be determined. Overall this study underscores that stem cell therapy at optimal time frame is crucial to obtain maximal therapeutic effects that can restore functional deficits or stop the progression of AD & PD.

    Sessions:
    Animal Models for Alzheimer and Neurodegeneration & Neuroimaging Approaches in Alzheimer Disease & Early Diagnosis

    Time:

    Title: Neurovascular Pathology in ApoB-100 Transgenic Mice

    Melinda E. Toth
    Hungarian Academy of Sciences, Biological Research Centre, Szeged, Hungary

    Biography
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    Biography

    Melinda E. Toth
    Hungarian Academy of Sciences, Biological Research Centre, Szeged, Hungary

    Melinda E. Tóth is currently a research associate scientist in the Institute of Biochemistry of the Biological Research Centre (Szeged, Hungary). She graduated from the University of Szeged with a master degree in biology in 2006. After graduation she continued her work in the lab of MiklósSántha, the Laboratory of Animal Genetics and Molecular Neurobiology as a PhD student and got her PhD from the University of Szeged in 2013. Her research interest is investigating the molecular basis of the protective role of heat shock proteins in diseases like Alzheimer’s disease and hyperlipidemia induced neurodegeneration in transgenic mouse models.



    Abstract
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    Abstract

    Melinda E. Toth
    Hungarian Academy of Sciences, Biological Research Centre, Szeged, Hungary

    Apolipoprotein B-100 (ApoB-100) is the major protein component of the low density and very-low-density lipoproteins that are responsible for cholesterol and triglyceride transport from the liver to the peripheral tissues. Therefore, the ApoB-100 overexpressing mouse strain is a frequently used model of atherosclerosis, as they are more susceptible to the cholesterol-enriched diet induced myocardial dysfunction. Moreover, previously we detected widespread neurodegeneration, neuronal apoptosis, synaptic dysfunction and tau-hyperphosphorylation in the brain of ApoB-100 transgenic mice finally leading to cognitive impairment. Since the neurovascular origin of various neurodegenerative diseases is becoming more and more accepted, our aim was to study the structural and functional impairments of the blood-brain barrier in ApoB-100 transgenic mice. In vivo permeability studies showed increased blood-brain barrier permeability in the hippocampus, while the disruption of the brain capillary endothelial tight junction structure and edematous swelling of astrocyte end-feet were demonstrated using transmission electron microscopy in transgenic brains. We found decreased P-glycoprotein (Abcb1) and vimentin immunostainings and altered Gfap immunostaining pattern related to the neurovascular unit by confocal microscopy. Real-time PCR showed increased Lox-1, Aqp4, and decreased Meox-2, Mfsd2a, Abcb1a, Lrp2, Glut-1, Nos2, Nos3 gene expression level in isolated microcapillary fraction of transgenic mice. These results underline the neurovascular origin of neurodegeneration in hypertriglyceridemicApoB-100 transgenic mice. This study was supported by the Hungarian Scientific Research Fund – OTKA (OTKA NN- 111006) and NRDI Office Hungary (GINOP-2.3.2-15-2016-00060).

    Time:

    Title: MRI Lateralization Index of Hippocampal Subfields Could Characterize Progression of Mild Cognitive Impairment to Alzheimer’s Disease

    Alessia Sarica
    Magna-Graecia University of Catanzaro, Italy

    Biography
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    Biography

    Alessia Sarica
    Magna-Graecia University of Catanzaro, Italy

    Alessia Sarica is currently a Post-doc Research-Fellow at Neuroscience Research Center, Department of Medical and Surgical Sciences, Magna-Graecia University of Catanzaro, Italy. She ownsa PhD in Biomedical and Computer Science Engineering and her research interests are on knowledge discovery from Neuroimaging, pattern-recognition and machine-learning. She has wide expertise in Random Forest and presented a systematic review about it for the prediction of Dementia (Sarica et al., 2017). She was the organizer and Special Guest Editor of a special issue on Journal of Neuroscience Methods:“A Machine learning neuroimaging challenge for automated diagnosis of Mild Cognitive Impairment” (Sarica et al., 2018).



    Abstract
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    Abstract

    Alessia Sarica
    Magna-Graecia University of Catanzaro, Italy

    A plethora of neuroimaging studies reported significant asymmetry of hippocampus in Alzheimer’s disease (AD), indicating that difference in volumes between left and right exists and varies with disease progression. However, few works investigated whether asymmetries of hippocampi could characterize the conversion of Mild Cognitive Impairment (MCI) to AD.Thus, aim of the present work was to evaluate the Lateralization Index (LI) of hippocampal substructures as MRI biomarker for differentiating stable (sMCI) from progressive MCI (pMCI). Two-hundred subjects were selected from ADNI, 100 sMCI (72.2yrs, MMSE 28) and 100 pMCI (72.4yrs, MMSE 27.3). The structural baseline T1swere processed with FreeSurfer 6.0 and volumes of hippocampi+12 subfields were extracted.Paired t-test was used for assessing significant differences between left and right, separately for sMCI and pMCI.The LI wascalculated as the absolute value of: ((Left-Right)/(Left+Right))*100. ANOVA adjusted for age, gender and intracranial volume was used for evaluating significant LI differences between sMCI and pMCI. The statistical threshold was Bonferroni corrected p<0.05/13=0.0038. Both sMCI and pMCIhad rightward asymmetries (right>left) in WH, CA1, CA3, CA4, GC_ML_DG, tail and HATA, and leftward(left>right)in presubiculum, while a rightward was found only in fissure and molecular layer of sMCI. The magnitude of LI was about 50% higherin pMCI than sMCI in the WH, subiculum and molecular layer. These preliminary findings showed that hippocampal LImaybe an early biomarker and that patients with stronger degree of asymmetry in these substructures had an increased risk of converting into AD.

    Time:

    Title: Amyloid-β Oligomers, Neuroinflammation and Novel Targets for Alzheimer’s Disease

    Michael Harte
    University of Manchester, United Kingdom

    Biography
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    Biography

    Michael Harte
    University of Manchester, United Kingdom

    Michael Harte is a neuropharmacology researcher currently working in the Division of Pharmacy & Optometry at the University of Manchester as a Senior Lecturer in Drug Action. Her lab specialises in the development of preclinical models of neuropsychiatric and neurodegenerative disorders for the testing of novel compounds for progression to the clinic. Her overall research goal is to develop improved preclinical models to advance our understanding of different CNS diseases and aid in the identification and testing of novel targets to ultimately improve treatment for patients.



    Abstract
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    Abstract

    Michael Harte
    University of Manchester, United Kingdom

    With current treatments for Alzheimer’s disease (AD) only providing temporary symptomatic benefits disease modifying drugs are urgently required. This approach relies on improved understanding of the early pathophysiology of AD. A new hypothesis has emerged, in which early memory loss is considered a synapse failure caused by soluble amyloid-β oligomers (Aβo). These small soluble Aβo, which precede the formation of larger fibrillar assemblies, may be the main cause of early AD pathologies. In support of this we have previously demonstrated the effects of an acute administration of LMW Aβo (SynAging) on cognitive, inflammatory, synaptic and neuronal markers in the rat [Watremez et al., 2018 Journal of Alzheimer’s Disease]. This model is very well established in our lab, is robust, reproducible and gives a measurable cognitive endpoint within 2 weeks. We have utilised this model for assessing symptomatic and / or neuroprotective effects of disease modifying drug candidates. It is becoming apparent that one such target, inflammation, is a key contributor to the progression of AD. In particular, on-going research is establishing the NLRP3-inflammasome complex as one of the most important regulators of inflammation, and that NLRP3 is central to the development of inflammation, pathology and memory deficits in rodent models for AD research. Our data point toward the NLRP3 inflammasome as a novel therapeutic target for AD.

    Time:

    Title: Prediction of Conversion to Alzheimer’s Disease in Individuals with Mild and Premild Cognitive Impairment with Machine Learning Algorithms

    Massimiliano Grassi
    Villa San Benedetto Menni Hospital, Como, Italy

    Biography
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    Biography

    Massimiliano Grassi
    Villa San Benedetto Menni Hospital, Como, Italy

    Massimiliano Grassi is senior data and research scientist at the Clinical Neurosciences Department of Villa San Benedetto Menni Hospital (Albese con Cassano, Como, Italy), cognitive psychoterapist and lecturer in statistics at the Istituto Superiore di Osteopatia (Milan, Italy). He is author of more than 15 scientific papers and his current research interest focuses on the application of machine learning techniques for the development of predictive algorithms and personalized medicine tools in field of the dementia and psychiatric disorders.



    Abstract
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    Abstract

    Massimiliano Grassi
    Villa San Benedetto Menni Hospital, Como, Italy

    No cure for Alzheimer’s Disease (AD) has been found yet. Early identification of which subjects at high risk, i.e. those with Mild Cognitive Impairment (MCI), will later develop AD is of key importance. This would allow making clinical trials of new AD treatments more cost-effective and valid, as well as beginning available therapies at an early stage of the disease progression. Several machine learning algorithms for the prediction of conversion to AD in subjects with MCI have been proposed. However, most of them either achieved only limited predictive accuracy or are based on expensive and hard-to-collect information. A novel algorithm for a prediction of a 3-year conversion to AD in MCI and PreMCI subjects will be presented. The prediction is based only on cost-effective and non-invasively collectable information, such as sociodemographic characteristics, neuropsychiatric and neuropsychological test scores, cardiovascular risk indexes, and clinician rated levels of brain atrophy. The algorithm was trained on a sample of 123 MCI/PreMCI subjects and achieved a cross-validated AUC of 0.962 and a balanced accuracy of 0.913 (MCI sub-group alone: AUC = 0.914, balanced accuracy = 0.874).An indirect evidence of its generalized accuracy obtained with a transfer learning approach will be also presented. In conclusion, our algorithm achieved very high performances outperforming the vast majority of currently available algorithms although it only employs predictors which can be non-invasively and cost-effectively assessed. Further testing and optimization in independent samples will finally warrant its trusted application in both clinical trials and clinical practice.

    Time:

    Title: Modulation of Beta-Amyloid Peptide Transporters on Brain-Blood Barrier by Ketogenic Diet

    Rita Businaro
    Sapienza University of Rome, Italy

    Biography
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    Biography

    Rita Businaro
    Sapienza University of Rome, Italy

    Rita Businaro, MD, PhD is a Professor of Human Anatomy in Faculty of Pharmacy and Medicine at Sapienza University of Rome, Italy. She is a Director of the II level Master in "Stress, Sport, Nutrition: New Diagnostic and Therapeutics Tools for Wellness, Fitness and Rehabilitation”. She is Vice-president of AIF (Italian Fulbright Association) and Member of ISNIM (International Society for NeuroimmunoModulation). She is also Coordinator of Erasmus Plus program. His main research topics is Study of comorbidity of Alzheimer's disease and cerebrovascular disorders: a multidisciplinary approach to identify cellular proteins and mechanisms involved in the accumulation of amyloid aggregates in the central nervous system, Cross-talk Central Nervous System-Immune System and Diet role in delaying Alzheimer's disease progression.



    Abstract
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    Abstract

    Rita Businaro
    Sapienza University of Rome, Italy

    Given the current absence of an effective pharmacologic treatment for Alzheimer’s disease (AD), the development of alternative therapeutic approaches (such as the ketogenic diet, KD) might be considered. The KD is a low-carbohydrate, high-fat diet based on the production of ketone bodies (KBs) in the blood. In view of the KD’s beneficial effects on the central nervous system and the lack of published data on the blood brain barrier (BBB), we used an invivo/in vitro approach to investigate the effect of the KD and KBs on the BBB. For the in vivo study, blood from 129Sv mice was assayed for beta-hydroxybutyrate and glucose dosage. Brain capillaries were isolated from mouse cortices, and RT-qPCR assays were used to evaluate the mRNA expression of transporters/receptors involved in the synthesis and transport of KBs, glucose and amyloid-beta (Aβ) peptide. The mRNA assays were also performed in an in vitro BBB model, based on brain-like endothelial cells (BLECs). After a ketotic state had been established and the BLECs’ integrity had been confirmed, we evaluated the mRNA expression of KB-, glucose- and Aβ-related genes. Lastly, the transport of fluorescently labelled Aβ-peptide across the BBB was studied after treatment with KBs. Our results showed that KBs regulate the expression of certain Aβ-peptide transporters/receptors and amyloid peptide-synthesizing enzymes. These data suggest that it is possible to modulate key molecular players in Aβ-peptide transport and synthesis at the BBB, and thus open up new perspectives for studying KB-related therapeutic approaches.

    Time:

    Title: Retinal Imaging of Misfolded Proteins in Alzheimer's

    Umur Kayabasi
    Uskudar University, Turkey

    Biography
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    Biography

    Umur Kayabasi
    Uskudar University, Turkey

    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 many papers in neuro-ophthalmology. He became an Assistant Professor at Uskudar University/Istanbul in 2016.



    Abstract
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    Abstract

    Umur Kayabasi
    Uskudar University, Turkey

    Introduction: Tau protein plays a crucial role in many neurodegenerative diseases including Alzheimer's disease (AD). Tau inclusions and amyloid beta (AB) depositions have been described in the post-mortem retina exams of AD patients. Cryo- electron microscopy (Cryo- EM) was recently used to detect the detailed structure of Tau filaments. Methods and Result: We examined the retinas of PET-proven live AD patients by spectral domain optical scanning tomography (SD- OCT) and fundusau to fluorescein (FAF). The hyper or hypo- fluorescent lesions in the retina were scanned by OCT and images that completely corresponded with the histopathological and Cryo- EM shapes of Tau filaments were observed. Conclusion: Retinal Tau is a very promising target to detect early changes in AD and retinal imaging may be an exciting and trust able technique to predict and monitor the disease.

    Time:

    Title: On the Role of APP in Acute (Stroke, Neurotrauma) and Chronic (Alzheimer's Disease) Neurodegeneration

    Anatoly Uzdensky
    South Federal University, Russia

    Biography
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    Biography

    Anatoly Uzdensky
    South Federal University, Russia

    Anatoly B. Uzdensky is a professor and a head of the Laboratory of Molecular Neurobiology at the Southern Federal University (Rostov-on-Don, Russia). He is the author of more than 120 journal papers and 3 books. His current research interests include stroke and neurotrauma, neurodegeneration and neuroprotection, cell biology, cell signaling and proteomics.



    Abstract
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    Abstract

    Anatoly Uzdensky
    South Federal University, Russia

    Accumulation of beta-amyloid (Aβ) in the brain cortex due to proteolysis of amyloid precursor protein (APP) leads to chronic neurodegeneration in Alzheimer’s disease. APP overexpression is also involved in pathophysiology of acute brain damage such as neurotrauma and ischemic stroke. We used protein microarrays to study changes in expression of signaling and neuronal proteins in the penumbra (2-mm ring around the infarction core) 1-24 hours after photothrombotic stroke in the rat brain cortex (ischemic stroke model). Among other biochemical changes (overexpression of pro- and antiapoptotic proteins, signaling proteins, actin cytoskeleton elements, and downregulation of tubulin and cytokeratins, and proteins involved in vesicular transport and synaptic processes), we observed overexpression of APP; nicastrin (component of γ-secretase); Aβ fragment (13-28); LRP1 (APOE receptor) and TMP21 that regulate APP proteolysis and Aβ release. Therefore, APP is rapidly accumulated and processed and in penumbra after acute brain damage. APP is also known to accumulate in injured nerves. We hypothesize the functional, probably, protective role of APP in dying neurons. In different pathogenic situations Intracellular APP fragment AICD can release and function as a transcription factor to regulate the expression of APP and other proteins. In chronic diseases such as Alzheimer’s disease death of individual neurons can occur similarly during few hours. Aβ release may be not harmful during short time intervals, but its aggregation can delay or prevent proteolysis and lead to Aβ accumulation, formation of amyloid plaques and neurodegeneration for years and dozens of years. Grant #6.4951.2017/6.7 Minobrnauki, Russian Federation.

    Sessions:
    Normal Brain Aging & Dementia with Lewy Bodies & Memory Disorders & Neurologic Problems & Neuropsychology & Neuropathology

    Time:

    Title: Why Physical Exercise Is the Best Way to Rejuvenate Ageing Brains

    Sonata Yau
    Hong Kong Polytechnic University, Hong Kong

    Biography
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    Biography

    Sonata Yau
    Hong Kong Polytechnic University, Hong Kong

    Dr. Sonata Yau obtained her Bachelor degree in Biochemistry from the Hong Kong University of Science and Technology in 2005, followed by a PhD in neuroscience in Department of Anatomy at The University of Hong Kong in 2009. She was awarded with several postdoctoral fellowships, research fellowships, conference travel awards and outstanding presentation awards. Before joining the Department of Rehabilitation Sciences, Hong Kong Polytechnic University, she worked as a postdoctoral fellow in the Division of Medical Sciences, University of Victoria, Canada. She is interested in studying the neural basis of pharmacological and non-pharmacological interventions that promote brain function in different disease animal models.



    Abstract
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    Abstract

    Sonata Yau
    Hong Kong Polytechnic University, Hong Kong

    With the rapid increase in the ageing population worldwide, tackling brain ageing is one of the most challenging contemporary health issues. Despite the huge long-term investment in the search for drugs that can delay or prevent aging-associated cognitive decline, the currently available pharmaceutical treatments are only modestly effective. The human brain possesses remarkable neuroplasticity (which refers to the brain’s ability to reorganize its structure and function in response to environmental stimulation), even later in life. Physical exercise is known to be the best medicine to improve brain health throughout an individual’s lifespan. Higher levels of physical activity are associated with better brain function, such as improved cognition learning and memory performance, especially in aged brains, suggesting physical exercise could be a non-pharmacological intervention for boosting capability of brain plasticity. In this talk, I will highlight the beneficial effects of physical exercise on promoting neuroplasticity in the hippocampus, a brain important for learning and memory and emotion regulation. I will also introduce the latest discoveries in animal research reporting the biological basis in which physical exercise influences hippocampal function, which is linked to cognitive and neuropsychiatric disorders, such as depression.

    Time:

    Title: Age- And Gender-Linked Differences in MRI Lateralization Index of Hippocampal Subfields

    Alessia Sarica
    Magna-Graecia University of Catanzaro, Italy

    Biography
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    Biography

    Alessia Sarica
    Magna-Graecia University of Catanzaro, Italy

    Alessia Sarica is currently a Post-doc Research-Fellow at Neuroscience Research Center, Department of Medical and Surgical Sciences, Magna-Graecia University of Catanzaro, Italy. She ownsa PhD in Biomedical and Computer Science Engineering and her research interests are on knowledge discovery from Neuroimaging, pattern-recognition and machine-learning. She has wide expertise in Random Forest and presented a systematic review about it for the prediction of Dementia (Sarica et al., 2017). She was the organizer and Special Guest Editor of a special issue on Journal of Neuroscience Methods:“A Machine learning neuroimaging challenge for automated diagnosis of Mild Cognitive Impairment” (Sarica et al., 2018).



    Abstract
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    Abstract

    Alessia Sarica
    Magna-Graecia University of Catanzaro, Italy

    Asymmetry of hippocampus is relevant in neurological diseases, however asymmetry of its substructures is poorly investigated in general population, and few is known about the normal-aging variations. For this reason, we explored differences in laterality index (LI) between females and males, and the correlation of LI subfields with age.One-hundred healthy subjects were selected from ADNI, 52 females (72.6yrs) and 48males (age 74.2yrs). The structural baseline T1swere processed with FreeSurfer 6.0 andvolumes of hippocampi and 12 subfields were extracted.Paired t-test was used for assessing differences in left and right, separately for females and males. The LI was calculated as absolute value of:((Left-Right)/(Left+Right))*100. ANOVA adjusted for ageand intracranial volume (ICV) was used for evaluating LI differences between groups. The correlation between age and LIs was investigated by linear regression with ICV as covariate. The statistical threshold was Bonferroni corrected p<0.05/13=0.0038. Both females and maleshad rightward asymmetries (right>left)in WH, CA1, CA3, CA4, GC_ML_DG, molecular layer, tail and HATA,while aleftward asymmetry (left>right) was found only in presubiculum of males. Males had higher asymmetry degree than females in parasubiculum (+30%) and tail (+20%), even if differences did not survive at Bonferroni’s. Only males presented association survived at Bonferroni’s between age and LI of WH, molecular layer and tail.Our findings showed that males had higher asymmetry magnitude than females,which increases with normal aging and we suggest that age and sex should be considered when evaluating hippocampal subfields laterality, especially when pathologies are studied.

    Time:

    Title: PSEN1 Expression is Associated to Promoter Methylation in the Brain of Alzheimer’s Mice and in Humans

    Andrea Fuso
    Sapienza University of Rome, Italy

    Biography
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    Biography

    Andrea Fuso
    Sapienza University of Rome, Italy

    Andrea Fuso, Ph.D., biologist, is researcher at Sapienza University of Rome. He teaches at post-graduations courses and is author of several scientific papers, book chapters and is speaker at many lectures and conferences. He serves in editorial boards, as referee for journals and grant committees and in the Board of Directors of the Epigenetics Society. His researches focus on neurodegenerative diseases, one-carbon metabolism and methylation reactions, studying the dynamics of DNA methylation/demethylation and then on-CpG methylation, applied to nutrition and one-carbon metabolism in neurodegeneration and muscle differentiation.



    Abstract
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    Abstract

    Andrea Fuso
    Sapienza University of Rome, Italy

    Presenilin1 (PSEN1) protein constitutes the catalytic subunit of the γ-secretase complex. This enzyme, among other, is responsible for the processing of the amyloid βprotein precursor (AβPP), eventually leading to the production and accumulation of the amyloid β (Aβ) peptides in the brain, associated with the Alzheimer’s Disease (AD). PSEN1 and γ-secretase are also responsible for the processing of key molecules (E-cadherin, Notch1) in course of neurodevelopment. Depicting the regulation of PSEN1 could be useful for the comprehension of the molecular mechanisms underlying neurodevelopment and neurodegeneration. Previous studies indicated PSEN1 as a locus subject to differential methylation in Alzheimer’s Disease affected subjects versus healthy controls. Moreover, we previously demonstrated that PSEN1 methylation and, consequently, expression are modulated by perturbation of the methylation metabolism in AD mice. The present study allowed to characterize the DNA methylation profile of PSEN1 promoter during the neurodevelopment and neurodegeneration, in the frontal cortex of TgCRND8 AD transgenic mice and of human subjects. The data obtained, allowed to demonstrate that both CpG and non-CpG (CpA, CpC, CpT) methylation of PSEN1 promoter is differentially modulated during development and aging and in AD patients versus controls. PSEN1 expression was correlated to CpG and non-CpG methylation patters. Altogether, these data point-out that non-CpG methylation has a functional role in PSEN1 regulation and stress the hypothesis that AD may have an epigenetic basis.

    Time:

    Title: Presenilin1 FAD Mutations Inhibit Neovascularization and Increase Vulnerability of Brain to Ischemia

    Anastosios Georgakopoulos
    Icahn School of Medicine at Mount Sinai, USA

    Biography
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    Biography

    Anastosios Georgakopoulos
    Icahn School of Medicine at Mount Sinai, USA

    Anastosios Georgakopoulos is a Research Associate Professor at the Center for Molecular Biology and Genetics of Neurodegeneration, department of Psychiatry at Icahn School of Medicine at Mount Sinai. Her laboratory studies mechanisms of ephrinB/EphB-mediated angiogenesis and neuroprotection and the role that Presenilin1/γ-secretase system has on their regulation aiming to discover methods to treat and prevent neurodegenerative disorders like AD. He had been working on the molecular biology of Presenilin1 for 20 years. He found the interaction of Presenilin1 with substrates of γ-secretase such as E- and N-cadherins, ephinB ligands and EphB receptors and the physiological role that these interactions may have.



    Abstract
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    Abstract

    Anastosios Georgakopoulos
    Icahn School of Medicine at Mount Sinai, USA

    A large amount of evidence has linked brain vascular disorders to the onset of Alzheimer’s Disease (AD). AD brains show impaired brain vasculature with changes in the microvasculature preceding neurodegenerative changes and cognitive decline. The changes in vasculature can be caused by a variety of factors including decreased angiogenesis. Insufficient angiogenesis and vascular regression in the AD brain may represent an important pathogenic mechanism ultimately affecting neuronal health. We observed that Presenilin1 (PS1) a protein involved in the pathogenesis of familial AD (FAD) promotes the angiogenic response of endothelial cells in vitro and that mutants of PS1 linked to FAD inhibit this function. We also found that a PS1 FAD mutant impairs brain neovascularisation after ischemic insult, a toxic stress known to induce angiogenesis, and that this mutant increases neuronal death induced by ischemia. MCAO-induced neovascularization, cerebral blood flow (CBF) and neuronal survival as measured by Collagen-IV immunostaining, perfusion MRI and NeuN immunostaining respectively were significantly decreased in FAD brains compared to WT. In addition VE-cadherin/Rok-α/Raf -1 angiogenic complexes, which regulate angiogenesis and which we have found to depend on PS1/γ- secretase, were decreased in brain extracts of PS1 FAD mutant mice compared to WT controls suggesting that PS1 regulates this angiogenic pathway in vivo and that PS1 FAD mutants impair brain angiogenesis. Together our data indicate that in FAD, brain vasculature is compromised due to defective angiogenesis, rendering the brain more vulnerable to toxic insults with reduced ability to recover leading to increased cell death and neurodegeneration.

    Time:

    Title: The expression and Activity of KV3.4 Channel Subunits are Precociously Upregulated in Astrocytes Exposed to Aβ Oligomers and in Astrocytes of Alzheimer's Disease Tg2576 Mice

    Anna Pannaccione
    University of Naples Federico II, Italy

    Biography
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    Biography

    Anna Pannaccione
    University of Naples Federico II, Italy

    Anna Pannaccione is the Assistant Professor of Pharmacology at the Department of Neuroscience of the University of Naples Federico II, School of Medicine from 2004. The main research themes are focused on the functional, pathophysiological and pharmacological role(s) of diverse classes of ionic channels and transporters. Throughout the years, these themes have been pursued by means of an integrated approach using electrophysiological, biochemical, genetic, and pharmacological techniques. In particular, the following research themes have been addressed to the characterization of the involvement of ionic homeostasis dysregulation in Alzheimer’s disease with particular attention to the study of sodium/calcium exchanger, voltage-gated potassium KV3.4/mirp2, and sodium NaV1.6 channels.



    Abstract
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    Abstract

    Anna Pannaccione
    University of Naples Federico II, Italy

    Astrocyte dysfunction emerges early in Alzheimer's disease (AD) and may contribute to its pathology and progression. Recently, the voltage gated potassium channel KV3.4 subunit, which underlies the fast-inactivating K+ currents, has been recognized to be relevant for AD pathogenesis and is emerging as a new target candidate for AD. In the present study, we investigated both in in vitro and in vivo models of AD the expression and functional activity of KV3.4 potassium channel subunits in astrocytes. In primary astrocytes biochemical, immunohistochemical, and electrophysiological studies demonstrated a time-dependent upregulation of KV3.4 expression and functional activity after exposure to amyloid-β (Aβ) oligomers. Consistently, astrocytic KV3.4 expression was upregulated in the cerebral cortex, hippocampus, and cerebellum of 6-month-old Tg2576 mice. Further, confocal triple labeling studies revealed that in 6-month-old Tg2576 mice, KV3.4 was intensely coexpressed with Aβ in nonplaque associated astrocytes. Interestingly, in the cortical and hippocampal regions of 12-month-old Tg2576 mice, plaque-associated astrocytes much more intensely expressed KV3.4 subunits, but not Aβ. More important, we evidenced that the selective knockdown of KV3.4 expression significantly downregulated both glial fibrillary acidic protein levels and Aβ trimers in the brain of 6-month-old Tg2576 mice. Collectively, our results demonstrate that the expression and function of KV3.4 channel subunits are precociously upregulated in cultured astrocytes exposed to Aβ oligomers and in reactive astrocytes of AD Tg2576 mice.

    Time:

    Title: Nuclear Envelope and Nuclear Pore Complex in Oxidative Stress, Aging and Neurodegeneration

    Jerzy Leszek
    Wroclaw Medical University, Poland

    Biography
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    Biography

    Jerzy Leszek
    Wroclaw Medical University, Poland

    Dr Jerzy Leszek is Professor of Psychiatry, Vice-Head of the Department of Psychiatry, Head of Alzheimer’s Disease Lab at the Medical University in Wroclaw, and Scientific Director of Alzheimer’s Disease Center in Scinawa near Wroclaw, Poland. He graduated at Medical University of Wroclaw in 1979, was awarded a doctorate in Wroclaw in 1981 and in 1999- examination for the degree of associate professor of psychiatry and since 2005 he is working as full professor of psychiatry at Wroclaw Medical University. He is author and co-author more than 250 papers (especially from old age psychiatry), some chapters to the books published in reputed Polish and international journals and serving as an editorial board member of several journals .He is Editor –in-Chief of Journal of Yoga and Physical Activity. He is Scientific Editor and co-author of first Polish academic handbook on Alzheimer’s disease and ten another academic handbooks from old age psychiatry (Polish and internationals) , member a lot of scientific associations e .g founder and president of Lower Silesian Association of Alzheimer’s Families, first of its kind in Poland ,President of the Scientific Council of Alzheimer’s Disease Center in Scinawa, near Wroclaw , Former President and founder of Polish Psychogeriatric Association, Former Secretary(now member) of European Old Age Psychiatry and Former Member of Board of Directions of International Psychogeriatric Association.



    Abstract
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    Abstract

    Jerzy Leszek
    Wroclaw Medical University, Poland

    The majority of enzymes and their substrates engaged in cells’ proliferation, differentiation and other vital functions shuttled between intranuclear and cytosolic compartments through the nuclear pore complexes, aqueous channels formed by multicomponent protein complexes of the nuclear envelope, also called nucleoporins. The nuclear pore protein complexes regulate movement of cell components from cytosol to nucleus and vice versa. Defective nucleoporin function could lead to inappropriate localization of a large number of nuclear and cellular components. Nucleoporin composition and structure are significantly age-dependent and cells lose essential nucleopore proteins with age.Oxidative stress applied to cells in culture caused marked changes in phosphorylation and 0-glycosylation of nucleoporin proteins, and altered their localization and interaction with other transport components, Such changes of the nuclear pore complex structure and function cold lead to aberrant intracellular trafficking of cell cycle regulating proteins and signaling proteins. Currently, growing body of evidence (and our seech) reveals that disturbances of nucleoporin structure and function are regular feature of degenerating neurons and could be responsible, in a major part, for the patho mechanism of neurodegeneration.

  • Keynote Speaker

    Time:

    Title

    Title: The Enigma of Eroom’s Law and The Wall Street Math Stifling Alzheimer’s Drug Discovery

    Max Tokarsky
    InvestAcure, USA
    Biography
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    Biography

    Max Tokarsky
    InvestAcure, USA

    Max Tokarsky is a Founder & CEO of InvestAcure, PBC. Max is a lifelong social entrepreneur and nonprofit executive. He is the Founder & CEO of InvestAcure, PBC, an SEC-approved RIA, with a bold plan to solve the current investment bottleneck at the clinical stage of Alzheimer's drug discovery. InvestAcure enables those impacted by Alzheimer's to partner in the search for a cure by automatically investing their spare in clinical stage pharmaceuticals spearheading research. This helps transition investment leadership from a narrow group of high-risk investors to a much larger and stable investment base, leading to more clinical trials, more drugs and drug combinations tested and progress to a cure.



    Abstract
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    Abstract

    Max Tokarsky
    InvestAcure, USA

    As the prevalence of Alzheimer’s disease (AD) grows, so do the costs it imposes on society. Yet, despite a significant number of drugs showing promise in animal models, progress is being stifled by a breakdown in the ROI model at the clinical stage of drug discovery. For complex diseases like Alzheimer's research, progress depends on the trial and error of real-world Phase 1 & 2 clinical trials. Due to the high cost of clinical research, this stage of drug discovery depends on industry-led investment. The average cost of developing a new drug, per billion US dollars spent on R&D, has doubled roughly every nine years since 1950. That means, adjusted for inflation, it costs 80 times more to develop a new drug today then it did in 1950! The observation of this trend was coined Eroom’s Law by industry analyst Jack Scannell in 2012, writing in Nature Reviews Drug Discovery. The current ROI from internal R&D in the pharmaceutical industry as a whole is an average 3.7%. For Alzheimer's, this model has broken down altogether and has led most major pharmaceuticals to downsize or close their Alzheimer’s research divisions. A structural solution to the current financial model is needed if we are to make progress to a cure. InvestAcure’s Public Benefit Corporation model offers one such solution, by transitioning investment leadership from the current Venture Capital model to micro-investment by those impacted by the disease.

    Keynote Speaker

    Time:

    Title

    Title: Inhibition of Endocytic Pathway of BACE1 as a Therapeutic Strategy for Alzheimer Disease Treatment

    Beka Solomon
    Tel Aviv University, Israel
    Biography
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    Biography

    Beka Solomon
    Tel Aviv University, Israel

    Professor Beka Solomon earned her Ph.D. in 1976 from the Weizmann Institute of Science, Rehovoth, Israel. She joined Tel-Aviv University in 1979 following post-doctoral studies and training periods at Harvard Medical School and Brigham and Women’s Hospital, Boston, USA. She is a member of the editorial board of Drugs of Today, Recent Patents on CNS Drug Discovery, of Neurodegenerative Diseases and Journal of Alzheimer's Disease. She was awarded the prestigious Zenith Award of the Alzheimer Association, and received the Dana Foundation Award for Neuroimmunology. In 2007 she was included in Scientific American’s List of 50 of the World’s Leading Innovators.



    Abstract
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    Abstract

    Beka Solomon
    Tel Aviv University, Israel

    Aims: Early endosomes are the first major sorting station in the endocytic pathway of BACE1 for cleavage of APP without interfering in processing of other vital substrates. The endocytic pathway is responsible for internalization and processing of cell surface APP which generates besides Aβ, the β- AICD capable of regulating transcription Here we propose to interfere with APP- BACE1 interaction, exploiting its presence at the cell surface prior to internalization into early endosomes. The proposed approach is based on antibodies blocking the β-secretase cleavage site of APP (BBS1).The complex APP-BBS1 is stable at acidic pH and may prevent the amyloidogenic processing of APP by BACE1 in early endosomes. Method: BBS1 antibodies raised against a chimera antigen containing only one Swedish mutation of APP, recognize both wild-type and mutated APP and do not bind to Aβ peptide. The effect of BBS1 on pathology and cognitive functions in mice model of AD was investigated. Results: The treatment of 3xTg-AD mice with BBS1 improved the cognitive function, lowered the levels of intracellular Aβ, reduce the plaques size, phosphorylated tau and inflammation .The antibodies down regulate apoptotic genes as P53 and GSK3β which are involved in neuronal apoptosis. Conclusion: Amyloid-β peptide is not the only active component for AD neurotoxicity and the β-AICD which regulates the transcription of genes involved in cytoskeletal dynamics and apoptosis contributing also to AD pathology. Inhibition of endocytic pathway of BACE1 via antibodies blocking the β-secretase cleavage site of APP may prevent amyloidogenic processing of APP and thus became a therapeutic strategy for AD treatment.

    Sessions:
    Alzheimers Disease & Dementia & Diagnosis & Prevention & Behavioural & Psychiatric Symptoms & Parkinson Disease & Huntington Disease

    Time:

    Title: Can We Currently Slow Down the Progression of Alzheimer’s Disease?

    Naji Tabet
    Brighton & Sussex Medical School, United Kingdom

    Biography
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    Biography

    Naji Tabet
    Brighton & Sussex Medical School, United Kingdom

    Naji Tabet is a Reader at Brighton and Sussex Medical School, United Kingdom and an Honorary Consultant in Old Age Psychiatry. His clinical and research interests and expertise are in the field of dementia. He and his team are investigating non-pharmacological interventions, lifestyles factors and co-morbid physical illnesses in relation to disease progression.Current research includes areas such as sleep, bilingualism, diet and exercise in dementia. Tabet has also been the Chief and Principal Investigator on nearly 30 Phase II-IV pharmacologically sponsored clinical studies assessing new treatment and diagnostic modalities in dementia disorders.



    Abstract
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    Abstract

    Naji Tabet
    Brighton & Sussex Medical School, United Kingdom

    Currently there is no cure for Alzheimer’s disease and available pharmacological treatment is at best symptomatic and does not work for everyone. Further, all randomised clinical trials testing disease modifying treatments have failed although many anti-amyloid and anti-tau drugs are still in phase II and III phases clinical trials. This talk will first concentrate on available treatments and will assess whether memory enhancers’ use is being currently optimised for patients. In recognition of the limitations of current treatment, the talk will then systematically assess non-pharmacological interventions in patients already diagnosed with Alzheimer’s disease to assess whether there is any evidence of efficacy. The evidence presented will be obtained from systematic reviews as well as the speakers group own work in exercise, diet and bilingualism (as a measure of cognitive reserve). Non-pharmacological interventions discussed will include exercise, diet, social networks, bilingulaism and sleep. It may be possible that by maximising currently available treatments and enhancing life style interventions for patients with mild to moderate Alzheimer’s disease that we may be able to improve the health and the quality of life for patients and at least slow down some of the disturbing associated symptoms.

    Time:

    Title: Multifaceted Properties of Human Serum Albuminas a Potential Therapeutic Approach to Treat Alzheimer's Disease

    Beka Solomon
    Tel Aviv University, Israel

    Biography
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    Biography

    Beka Solomon
    Tel Aviv University, Israel

    Professor Beka Solomon earned her Ph.D. in 1976 from the Weizmann Institute of Science, Rehovoth, Israel. She joined Tel-Aviv University in 1979 following post-doctoral studies and training periods at Harvard Medical School and Brigham and Women’s Hospital, Boston, USA. She is a member of the editorial board of Drugs of Today, Recent Patents on CNS Drug Discovery, of Neurodegenerative Diseases and Journal of Alzheimer's Disease. She was awarded the prestigious Zenith Award of the Alzheimer Association, and received the Dana Foundation Award for Neuroimmunology. In 2007 she was included in Scientific American’s List of 50 of the World’s Leading Innovators.



    Abstract
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    Abstract

    Beka Solomon
    Tel Aviv University, Israel

    Alzheimer's disease is neurodegenerative disorder involving many related and interdependent pathologies that manifests simultaneously. No treatment is currently available; however, an agent addressing several key pathologies simultaneously has a better therapeutic potential. Human serum albumin (HSA) is a highly versatile protein, harboring multifunctional properties that are relevant to key pathologies. HSA decreased with aging and is associated with cognitive impairment in the elderly, further implicating its involvement in AD.HSA affect AD pathologies from several different aspects such as antioxidant activity, detoxification, anti-inflammatory properties, reduce BBB permeability and promote neuronal survival. All of these properties have significance in relation to AD pathology especially it interacts directly with amyloid beta peptide (Aβ), one of the hallmark pathologies in AD. HSA and Aβ interaction in vitro, show that HSA can reduce oligomeric Aβ and induced cellular stress in vitro due to direct binding to Aβ rather than other properties of HSA. In vivo, we treat the mice with pumps infusing HSA intracerebroventricularly(ICV),in an AD 3xTg mice model. A significant effect on amyloid-β (Aβ) pathology was observed. Aβ1-42, soluble oligomers, and total plaque area were reduced.as well as Total and hyperphosphorylated tau. HSA treatment also reduced brain inflammation, affecting both astrocytes and microglia markers. Finally, evidence for blood-brain barrier and myelin integrity repair was observed The work presented here shedding light over the mechanism of HSA and Aβ interaction anddemonstrate that ICV administration of HSA is a potential therapeutic approach with multifaceted beneficial effects to treat AD

    Time:

    Title: The Functional Ramifications of TREM2 Variants in Human Induced Pluripotent Stem Cell Derived Microglia-like Cells

    Jennifer M Pocock
    University College London Institute of Neurology, United Kingdom

    Biography
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    Biography

    Jennifer M Pocock
    University College London Institute of Neurology, United Kingdom

    Jennifer Pocock hold a degree in Applied Biology (1st class, specializing in Cell Biology, Biochemistry and Physiology) and a PhD in Neurophysiology. She had undertaken postdoctoral research at the University of Dundee, Scotland, UK and the University of California, USA. She is currently a Senior Lecturer in the Department of Neuroinflammation, University College London Institute of Neurology, London, UK. His research focus is to understand the role of inflammatory particularly microglia, the immune cell of the brain, in disease progression, especially in Alzheimer’s Disease. His laboratory is currently using human fibroblast derived iPSCs expressing mutations in the TREM2 receptor, linked to Alzheimer’s disease (R47H), Nasu Hakola disease (T66M, W50C) as well as CRISPR edited BV2 microglia for TREM2 KD and KO with which we are investigating signalling pathway deviations from control common variant cells.



    Abstract
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    Abstract

    Jennifer M Pocock
    University College London Institute of Neurology, United Kingdom

    The dysfunction of microglia, the brain’s immune cells, is linked to dementia. Heterozygous variants in the gene Triggering Receptor Expressed on Myeloid Cells (TREM2)are associated with late-onset Alzheimer’s disease, whilst homozygous variants cause Nasu-Hakola disease (NHD), an early-onset dementia. Here, we generated induced pluripotent stem cell-derived microglia-like cells (iPSC-MGLC) from patients with NHD caused by a homozygous T66M or W50C variant in the TREM2 gene, unaffected T66M heterozygous relatives and controls. Human iPSC-MGLC expressed microglial markers, and expressed and secreted TREM2. TREM2 expression and secretion were reduced in TREM2 variant iPSC-MGLC, which also exhibited impaired phagocytosis of apoptotic neuronal cells, but not other substrates. Cytokine secretion was unaffected. Taken together, these findings highlight the ramifications of TREM2 variants in robust human models of microglia.

    Time:

    Title: Pathogenic Role of FcγRIIb in Amyloid and Tau Pathogenesis in Alzheimer’s Disease

    Yong-Keun Jung
    Seoul National University, Korea

    Biography
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    Biography

    Yong-Keun Jung
    Seoul National University, Korea

    Yong-Keun Jung obtained his Ph.D from the Albert Einstein College of Medicine, NY, USA at 1993. From 1993-1996, he was a post-doctoral fellow in the department of cell biology, Harvard Medical School, USA. He then returned to Korea and is now a professor at Department of Biological Science, Seoul National University (SNU), Korea. He contributed to elucidation of the cell death machinery and our understanding of its association with human disease. In particular, the role of cell death and autophagy in the pathogenesis of human disease, including Alzheimer’s disease, ischemia and cancer etc, is being investigated.



    Abstract
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    Abstract

    Yong-Keun Jung
    Seoul National University, Korea

    Amyloid-beta (Aβ) induces neuronal loss and cognitive deficits and is believed as a prominent cause of Alzheimer’s disease (AD). However, cellular mechanism of the pathogenesis is not fully understood. Here we show that Fcgamma-receptor IIb (FcγRIIb) mediates Aβ neurotoxicity and neurodegeneration. We found that FcγRIIb is a receptor of Aβ1-42 oligomers and genetic depletion of FcγRIIb rescues the memory impairments in AD model mice. In addition, the FcγRIIb-SHIP2 axis is critical in Aβ1-42-induced tau pathology. Fcgr2b knockout or antagonistic FcγRIIb antibody inhibited Aβ1-42-induced tau hyperphosphorylation and rescued memory impairments in AD mouse models. As a action model, SHIP2 is recruited into phosphorylated FcγRIIb to affect PtdIns(3,4)P2 metabolism for tau phosphorylation. Further, targeting SHIP2 expression by lentiviral siRNA in 3xTg-AD mice or pharmacological inhibition of SHIP2 potently rescued tau hyperphosphorylation and memory impairments. Thus, we conclude that the FcγRIIb-SHIP2 axis links Aβ neurotoxicity to tau pathology by dysregulating PtdIns(3,4)P2 metabolism, providing insight into therapeutic potential against AD. More, emerging evidences suggest that intraneuronal Aβ correlates with the onset of Alzheimer’s disease (AD) and highly contributes to neurodegeneration. Our findings illustrate that FcγRIIb2 is essential for neuropathogenic function of Aβ in AD.

    Time:

    Title: Neuroprotective Effect of Chia Seeds Extract on Aluminum Chloride Induced Alzheimer’s Rat Model

    Eman Abdelnaby
    Cairo University, Egypt

    Biography
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    Biography

    Eman Abdelnaby
    Cairo University, Egypt

    Eman H. Abdelnaby is an Ethologist who has graduated from Cairo University, Egypt. She has earned her Master's in Animal Behavior. She is currently enrolled in her PhD in Alzheimer's Disease (AD), her study is about developing new herbal approaches (natural antioxidants) in AD Rat model. She was a professional fellow that visited several academic institutions as a scholar, including MBNI and ULAM-Michigan University, MSU- USA. Also joined an AD scientific project as an Erasmus+ student at Alexandru Ioan Cuza University, Romania. She has more than 7 years of research and teaching experience as an assistant lecturer and academic advisor. She is also a Certified Life Coach, a Certified Professional Trainer accredited from Missouri State University and a member of the "Board of International Trainers”, and currently acting as a Mentor at MENA-Michigan Initiative for Global Action through Entrepreneurship (M2GATE) program.



    Abstract
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    Abstract

    Eman Abdelnaby
    Cairo University, Egypt

    Alzheimer’s disease (AD) is the most common form of dementia, associated with irreversible neuropathological and neurobehavioral changes accompanied by memory and cognitive impairments. Despite the overwhelming evidence that links oxidative stress and AD, antioxidant therapies have limited success in clinical trials.The present study was aimed to evaluate the protective effect of Chia seeds extract on aluminum chloride (AlCl3) induced rat model. Oral administration of AlCl3 (200 mg/kg) for 60 days significantly elevated the levels of aluminum (Al), activity of acetylcholinesterase (AChE) and protein expressions of amyloid precursor protein (APP) compared to control group in hippocampus and cortex of rat brain. Chia seeds extract was administrated orally along with AlCl3 for 60 days (day after day protocol), significantly revert the Al concentration, AChE activity and Ab synthesis-related molecules in the studied brain regions. Our results showed that the behavioral impairments caused by aluminum were significantly attenuated by Chia seeds extract. As the spontaneous locomotor and exploratory activities in open field test were significantly reduced and the learning and memory impairments in Novel Object Recognition (NOR) test were enhanced. The histopathological studies in the hippocampus and cortex of rat brain also supported that Chia seeds extract markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. From these results, it is concluded that Chia seeds can reverse memory loss caused by aluminum intoxication through attenuating AChE activity and amyloidogenic pathway.

    Time:

    Title: Copper Homeostasis in Relation to Cognitive Dysfunction in Neurodegenerative Disorders

    Rosanna Squitti
    Istituto Centro San Giovanni di Dio- Fatebenefratelli, Italy

    Biography
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    Biography

    Rosanna Squitti
    Istituto Centro San Giovanni di Dio- Fatebenefratelli, Italy

    Rosanna Squitti, PhD, works in Italy with Fatebenefratelli Institutes, and she is visiting Scholar at the University of Miami (Fl, US). She is author of more than 100 peer reviewed publications and 2 patents. She contributed to the understanding of Alzheimer’s disease (AD) by demonstrating the existence of a copper imbalance in AD, consisting in systemic excess copper not bound to ceruloplasmin (non-Cp Cu) and decreased protein-bound copper in the brain. She demonstrated that ATP7B gene, which is a major regulator of non-Cp Cu levels, associates with the AD risk, supporting the existence of a Cu subtype of AD.



    Abstract
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    Abstract

    Rosanna Squitti
    Istituto Centro San Giovanni di Dio- Fatebenefratelli, Italy

    Trace metal dyshomeostasis has been linked to cognitive deterioration and in particular a disturbance in the regulation of copper (Cu). Excess Cu not bound to ceruloplasmin (non-Cp Cu, also referred to as ‘free’ Cu), is thought to play a role in the development of Alzheimer’s disease (AD). Non-Cp Cu is redox active and its toxicity results from its ability to accelerate oxidative stress via Fenton-like and Haber Weiss chemistry reactions. The plasma component of non-Cp Cu is composed of Cu loosely bound to albumin, transcuprein, peptides and amino acids and it is exchanged among them. It makes up 5-10% of plasmaCu in normal condition. If the non-Cp Cu pool becomes expanded, this Cu becomes toxic, as exemplified by Wilson’s disease and reported in AD and other neurodenerative diseases. Non-Cp Cu may serve as a biomarker for cognitive impairment in AD. Elevated levels of non-Cp Cu in serum increase the probability of having AD by approximately three-fold. Subjects with mild cognitive impairment (MCI, a prodromal stage of AD) have elevated non-CpCu levels and a hazard rate of conversion to AD three times higher than those with normal non-CpCu values. These results suggest that abnormalities of Cu act at early stages of the disease. This concept is further supported by the finding that an increased frequency of variants in the ATP7B gene, which is a major regulator of non-Cp Cu levels, associates with the risk (odds ratio from 1.63 to 5.16) of having AD. Non-Cp Cu appears to be increased also in Parkinson’s disease and in corticobasal degeneration but not in frontotemporal lobar dementia. Recent studies support the existence of a Cu subtype of AD, typified by increased levels of non-Cp Cu, exhibiting peculiar ATP7B gene, neurophysiological and neuroimaging patterns.

    Time:

    Title: Recombinant Human Hsp70 Exhibit a Significant Neuroprotective Effect in Two Mouse Models of Alzheimer’s Disease

    David Garbuz
    Engelhardt Institute of Molecular Biology, Russia

    Biography
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    Biography

    David Garbuz
    Engelhardt Institute of Molecular Biology, Russia

    David G. Garbuz was born in 1978. He is Student of Moscow Veterinary Academy from 1995– 2000. He is the PhD Student of Engelhardt Institute of Molecular Biology Russian Academy of Sciences from 2000 – 2003. He did PhD in molecular biology at 2004. He is a researcher at Engelhardt Institute of Molecular Biology RAS from 2003 – 2008. He did Postdoctorate at USA, New-York, NYU Medical Centre from 2008 – 2009. He is the Assistant Professor at Moscow Veterinary Academy from 2008 – 2011. At present he is a Senior Research Scientist at Engelhardt Institute of Molecular Biology RAS from 2009. He received the degree of Doctor of Biological Sciences, the highest scientific degree in Russia at 2018.



    Abstract
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    Abstract

    David Garbuz
    Engelhardt Institute of Molecular Biology, Russia

    Molecular chaperone Hsp70 plays protective role in various neurodegenerative disorders including Alzheimer's disease (AD). Our data suggest that human recombinant Hsp70 effectively crosses the blood-brain barrier when administrated intranasally and exhibits dramatic neuroprotective effect in the bilateral olfactory bulbectomy (OBX mice) and transgenic 5XFAD mouse models of AD-like neurodegeneration. Chronic treatment by recombinant Hsp70 leads to a decrease of beta-amyloid level and restores the neuron morphology and density in the temporal cortex and hippocampal regions. In both mouse models of AD recombinant Hsp70 restored cognitive functions including learning and memory. Besides, Hsp70 treatment normalizes a number of biochemical indicators of the state of the nervous system in the aged animals, including lipofuscin and synaptophysin levels. Using deep sequencing, we identified multiple differentially expressed genes (DEGs) in the hippocampus of transgenic and non-transgenic mice of different age groups. Importantly, the pattern of DEGs strongly depends on the transgenicity and age of the experimental animals. Thus, upregulation of inflammatory and proteasomal genes is a feature of old transgenic 5XFAD mice. This analysis also demonstrated that recombinant Hsp70 administration strongly modulates the spectrum of DEGs in transgenic animals, reverting it to a pattern similar to that observed in non-transgenic mice of the same age. These changes include upregulation of genes responsible for amine transport, transmission of nerve impulses, synaptic transmission, dopamine metabolic processes and other pathways that are impaired in transgenic 5XFAD mice. Overall, our data indicate that chronical Hsp70 treatment may be an effective therapeutic against neurodegenerative diseases of the Alzheimer's type.

    Time:

    Title: Diagnosis of the Home Care for Persons with Alzheimer in Portugal: Current Situation and Perspectives

    Eduardo Joao Ribeiro Santos
    University of Coimbra, Portugal

    Biography
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    Biography

    Eduardo Joao Ribeiro Santos
    University of Coimbra, Portugal

    Eduardo Santos is Associated Professor of Counseling Psychology at the College of Psychology and Education, University of Coimbra, Portugal, and Adjunct Professor at the State University of New York, at Albany, USA. He is the Scientific Coordinator of the research, development and innovation unit Institute of Cognitive Psychology, Human and Social Development, University of Coimbra, articulating with national and international institutions within postgraduate research and training fields. His current interests focus on systemic-developmental processes along the life-span with emphasis in biotechnopsychosocial perspectives. He is author of a large number of books, scientific articles, and presentations at national and international levels.



    Abstract
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    Abstract

    Eduardo Joao Ribeiro Santos
    University of Coimbra, Portugal

    The home care for patients with Alzheimer’s disease is an increasing clinical and social practice in the field of dementia and ageing. The goal of this study is to make a diagnosis of the situation in Portugal. The results of an online survey about this subject are presented, showing that in Portugal there are no sufficient and specialized answers, in what concerns assisted active living methodologies performed by interdisciplinary teams. From this evidence it is discussed how to implement efficient practices in order to offer care options for patients and caregivers.

    Time:

    Title: Copper Homeostasis in Frontotemporal Lobar Degeneration

    Rosanna Squitti
    Istituto Centro San Giovanni di Dio- Fatebenefratelli, Italy

    Biography
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    Biography

    Rosanna Squitti
    Istituto Centro San Giovanni di Dio- Fatebenefratelli, Italy

    Rosanna Squitti, PhD, works in Italy with Fatebenefratelli Institutes, and she is visiting Scholar at the University of Miami (Fl, US). She is author of more than 100 peer reviewed publications and 2 patents. She contributed to the understanding of Alzheimer’s disease (AD) by demonstrating the existence of a copper imbalance in AD, consisting in systemic excess copper not bound to ceruloplasmin (non-Cp Cu) and decreased protein-bound copper in the brain. She demonstrated that ATP7B gene, which is a major regulator of non-Cp Cu levels, associates with the AD risk, supporting the existence of a Cu subtype of AD.



    Abstract
    χ

    Abstract

    Rosanna Squitti
    Istituto Centro San Giovanni di Dio- Fatebenefratelli, Italy

    Trace metal dyshomeostasis has been linked to cognitive deterioration and in particular a disturbance in the regulation of copper (Cu). Excess Cu not bound to ceruloplasmin (non-Cp Cu, also referred to as ‘free’ Cu), is thought to play a role in the development of Alzheimer’s disease (AD). Non-Cp Cu is redox active and its toxicity results from its ability to accelerate oxidative stress via Fenton-like and Haber Weiss chemistry reactions. The plasma component of non-Cp Cu is composed of Cu loosely bound to albumin, transcuprein, peptides and amino acids and it is exchanged among them. It makes up 5-10% of plasma Cu in normal condition. If the non-Cp Cu pool becomes expanded, this Cu becomes toxic, as exemplified by Wilson’s disease and reported in AD and other neurodegenerative diseases. Elevated levels of non-Cp Cu in serum increase the probability of having AD by approximately three-fold. Meta-analyses show copper dyshomeostasis in Alzheimer’s disease. However, a study evaluating copper changes in other neurodegenerative forms of dementia has not yet been performed. In this study, we assessed copper, ceruloplasmin, copper not bound to ceruloplasmin and copper to ceruloplasmin ratio in 85 patients affected by Frontotemporal Lobar Degeneration (FTLD) and 55 healthy controls. Data were analysed through multivariate ANOVA models taking into account age and sex as covariates and the stratification for FTLD variants, after calculating power analysis to ensure the reliability of the conclusions drawn. The study revealed no difference between the groups.

    Time:

    Title: Cerebrospinal and Serum Alpha-synuclein Species as Potential Biomarkers for Parkinson’s Disease

    Omar El-Agnaf
    Hamad Bin Khalifa University, Qatar

    Biography
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    Biography

    Omar El-Agnaf
    Hamad Bin Khalifa University, Qatar

    Omar El-Agnaf is acting Executive Director at Qatar Biomedical Research Institute (QBRI) and Director of Neurological Disorders Research Center at QBRI. His primary research concerns neurodegenerative disease. Since he moved to the region, he has assembled an excellent research team and has been successful in attracting an array of scientific funding from prestigious international funding agencies. Dr. El-Agnaf is frequently invited as a speaker at international scientific and clinical meetings and is currently a member of the editorial board of several international journals. His track record of basic and translational research productivity is characterized by publications in high-ranking scientific journals. He is considered a pioneer in the field of Parkinson’s disease and related neurodegenerative diseases. Several inventions have emerged from his research and provided new insights into the molecular pathogenesis of neurodegenerative diseases and have offered new opportunities for the development of novel diagnostic and therapeutic tools for Parkinson’s disease and related disorders. His research has also been translated into clinical studies to evaluate novel markers as diagnostic tools for neurodegenerative diseases. He has been granted 8 patents and 6 under consideration, and published more than 120 refereed articles, with 52 h-index and total citations >8,600.



    Abstract
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    Abstract

    Omar El-Agnaf
    Hamad Bin Khalifa University, Qatar

    Developing effective treatments for neurodegenerative diseases is one of the greatest medical challenges of the 21st century. Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) are very common neurological disorders of the elderly. Although many of these clinical entities have been recognized for more than a hundred years, it is only during the past fifteen years that the molecular events that precipitate the diseases have begun to be understood. Mutations in the alpha-synuclein gene cause early-onset PD, often associated with dementia. Neuropathologically these diseases are characterized by the presence of Lewy bodies, intraneuronal inclusions mostly composed of alpha-synuclein protein fibrils. Despite the progress that has been made in understanding the underlying disease mechanisms of PD and DLB, there remains an urgent need to develop methods for use in diagnosis. The development of reliable surrogate markers for the presence and abundance of alpha-synuclein lesions (Lewy bodies) in the brain would naturally facilitate a more streamlined work-up during the early care of PD and DLB patients, and importantly, allow for the biologically guided evaluation of future drug trials aimed at neuroprotection in the synucleinopathies. In this seminar, I will present the progress which has been made so far by our group to explore the use of CSF α-synuclein and its modified forms as biomarkers for PD and related disorders.

    Time:

    Title: Dyskinesias-Reduced-Self-Awareness in Patients with Parkinson's Disease. A Neurocognitive Approach

    Sara Palermo
    University of Turin, Italy

    Biography
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    Biography

    Sara Palermo
    University of Turin, Italy

    Sara Palermo is MSc in Clinical Psychology and PhD in Experimental Neuroscience. She is Postdoc Research Fellow at the University of Turin, while she is ordinary member of the Italian Society of Neuropsychology and of the Italian Association of Psychogeriatrics. Importantly, she is a research member of the European Innovation Partnership on Active and Healthy Aging, for which she is involved in the Action Group A3 “Functional decline and frailty”. Sara Palermo is part of the Editorial Panel of “EC Psychology and Psychiatry” (ECPP), an internationally peer reviewed journal aimed to publish topics related to psychology and medicine.



    Abstract
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    Abstract

    Sara Palermo
    University of Turin, Italy

    Parkinson's disease (PD) patients may be partially or even completely unaware of the presence of involuntary movements in terms of dyskinesias-reduced-self-awareness (DRSA). As the association with executive dysfunction is a matter of debate and we hypothesize it plays an important role in DRSA, we previously analyzed the role of dopaminergic treatment on the medial-prefrontal-ventral-striatal circuitry using a neurocognitive approach. Indeed, we have given special attention to metacognitive abilities related to action-monitoring and other factors, such as "Theory of Mind", that represent a novel explanation of the phenomenon. Importantly, response-inhibition dysfunction is often observed in PD. Besides being involved in response-inhibition, the anterior cingulate cortex (ACC) is part of a functional system based on self-awareness and engaged across cognitive, affective and behavioral contexts. In a new study, we used an event-related fMRI to verify the association between response-inhibition disabilities and DRSA. The presence of DRSA was assessed using the DyskinesiasSubtracted-Index (DS-I). Cingulate functionality was evaluated with fMRI, while patients performed an ACC-sensitive GO-NoGO task. Association between blood oxygenation level dependent response over the whole-brain during the response-inhibition task and DS-I scores was investigated. The presence of DRSA result associated with a reduced functional recruitment in the bilateral ACC, bilateral anterior insular cortex and right dorsolateral prefrontal cortex (p <0.05). Moreover, DS-I scores significantly correlated with percent errors on the NoGO condition (r=.491, p=.009). These findings add evidence to the relevant role of executive dysfunctions in DRSA pathogenesis, with a key role played by ACC.

    Time:

    Title: Tau Protein in Oral Mucosa and Cognitive State: A Cross-Sectional Study

    Robert Norman
    Nova SouthEastern University, USA

    Biography
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    Biography

    Robert Norman
    Nova SouthEastern University, USA

    Dr. Robert A. Norman is a board-certified dermatologist and family practitioner who has been in practice for over 25 years. He is a Faculty member of Medicine in Department of Biochemistry at Autonomous University of San Luis Potosí, San Luis Potosí, Mexico.



    Abstract
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    Abstract

    Robert Norman
    Nova SouthEastern University, USA

    Neurodegenerative diseases are characterized by the presence of abnormal aggregates of proteins in brain tissue. Among them, the presence of aggregates of phosphorylated Tau protein (p-Tau) is the hallmark of Alzheimer’s disease (AD) and other major neuro-degenerative disorders such as corticobasal degeneration and frontotemporal dementia among others. Although Tau protein has previously been assumed to be exclusive to the central nervous system, it is also found in peripheral tissues. The purpose of this study was to determine whether there is a differential Tau expression in oral mucosa cells according to cognitive impairment. Eighty-one subjects were enrolled in the study and classified per Mini-Mental State Examination test score into control, mild cognitive impairment (MCI), and severe cognitive impairment (SCI) groups. Immunocytochemistry and immunofluorescence revealed the presence of Tau and four p-Tau forms in the cytoplasm and nucleus of oral mucosa cells. More positivity was present in subjects with cognitive impairment than in control subjects, both in the nucleus and cytoplasm, in a speckle pattern. The mRNA expression of Tau by quantitative real-time polymerase chain reaction was higher in SCI as compared with the control group (P <0.01). A significantly higher percentage of immunopositive cells in the SCI group was found via flow cytometry in comparison to controls and the MCI group (P <0.01). These findings demonstrate the higher presence of p-Tau and Tau transcript in the oral mucosa of cognitively impaired subjects when compared with healthy subjects. The feasibility of p-Tau quantification by flow cytometry supports the prospective analysis of oral mucosa as a support tool for screening of proteinopathies in cognitively impaired patients. Keywords: Tau protein, dementia, neurodegenerative diseases, alzheimer disease, oral mucosa cells

  • Sessions:
    Poster Session

    Time:

    Title: Weight Loss and Muscle Wasting May be Risk Factors of Falling Event in Patients with Parkinson’s Disease

    Sook-Keun Song
    Jeju National University Hospital, Korea

    Biography
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    Biography

    Sook-Keun Song
    Jeju National University Hospital, Korea

    Sook-Keun Song is an Associate Professor in Department of Neurology at Jeju National University Hospital. She is a Fellow, Division of movement disorders in Department of Neurology, Severance Hospital at Yonsei University College of Medicine. She completed her BS, Biology at Korea University. She did MS, Neurobiology at Pohang University of Science and Technical. She did MD in Yonsei University College of Medicine.



    Abstract
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    Abstract

    Sook-Keun Song
    Jeju National University Hospital, Korea

    Objective: To compare weight and body composition between patients with falling event and without falling event in non-demented Parkinson’s disease patients. Background & significance: Loss of body weight and muscle wasting are common in patients with Parkinson’s disease, and associated with symptoms and disease progression. The aim of this study was to explore the association between change of weight and body composition and falling events in non-demented patients with Parkinson’s disease Methods: This cross-sectional study was conducted on 49 patients with Parkinson’s disease from Jeju National University Hospital. We excluded patient with short follow-up period less than 12 months, with severe disease state (more than H&Y stage III), or with dementia. We measured the height, body weight, body mass index, abdominal circumference, and tight circumference. We divided the patient into two groups depending on the presence of falling event in the last six months. Assessment of age, disease duration, weight and body compositions between groups were analyzed using Mann-Whitney test. Results: 31 patients without falling event and 18 patients with falling event in last six months were enrolled. Age, disease duration, heights were not significantly different between patients with or without falling event. Patient without falling event had more weight but was not significant. Patients with falling event showed significantly low abdomen and thigh circumference (p<0.01). Conclusions: Weight loss and decreased abdomen and thigh circumference can be risk factor of falling event in non-demented patients with Parkinson’s disease.

    Time:

    Title: Effect of Lycoris Chejuensis and its Active Components on Experimental Models of Alzheimer’s Disease

    Hyun Ok Yang
    Korea Institute of Science and Technology, Korea

    Biography
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    Biography

    Hyun Ok Yang
    Korea Institute of Science and Technology, Korea

    Hyun Ok Yang has complete her PhD on pharmacognogy at Seoul National University in 1993. After Post-doctoral study at University of Iowa, USA, she is now a principal research scientist at Natural Products Research Center in Korea Institute of Science and Technology (KIST) & a professor of UST, KIST School, Republic of Korea.



    Abstract
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    Abstract

    Hyun Ok Yang
    Korea Institute of Science and Technology, Korea

    We found that an extract of Lycoris chejuensis, and its three isolated active components, narciclasine, 7-deoxynarciclasine and 7-deoxy-trans-dihydronarciclasine, each significantly reduced the formation of amyloid-β peptides in HeLa cells transfected with an amyloid precursor protein carrying the Swedish mutation up to 45±3.6%. The extract down-regulated amyloid precursor protein, especially the mature form by up to 88%, and reduced the ability of secretases to generate toxic amyloid-β. Double-transgenic mice treated with the extract for 4 months also showed significantly reduced levels of amyloid-β and plaques while exhibiting improved memory functions in the Morris water maze and novel object recognition tests. In conclusion, the extract and isolated active components of L. chejuensis decreased the production of amyloid-β by attenuating amyloid precursor protein levels. Furthermore, the extract improved the disrupted memory functions in animals while inhibiting amyloid plaque formation. Thus, this extract, as well as its active components, could prove beneficial in the treatment of Alzheimer’s disease. Keywords: Lycoris chejuensis, Alzheimer’s disease, Amyloid-beta, Amyloid-beta precursor protein, Narciclasine

    Time:

    Title: Ceftriaxone Improves Learning and Memory Deficits by Promoting Glutamate-Glutamine Cycle in Early Stage of the APP/PS1 Transgenic Mouse Model for Alzheimer's Disease

    WenBin Li
    Hebei Medical University, China

    Biography
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    Biography

    WenBin Li
    Hebei Medical University, China

    Wenbin Li is a Professor in the Department of Pathophysiology, Neuroscience Research Center, Hebei Medical University, China. He is now mainly interested in the fundamental study in the prevention and therapy of Alzheimer’s disease, cerebral ischemia and the mechanism of cerebral ischemia tolerance.



    Abstract
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    Abstract

    WenBin Li
    Hebei Medical University, China

    Alzheimer's disease (AD) is characterized by progressive impairment of learning, memory and cognitive functions. Glutamate as neurotransmitter plays an important role in learning, memory and cognition. The glutamate homeostasis and reutilization are associated with glutamate uptake by astrocytic glutamate transporter-1(GLT-1) and the subsequent glutamate-glutamine cycle. Increasing evidence showed the dysregulation of GLT-1 and glutamate-glutamine cycle in AD. Ceftriaxone (Cef) has been reported to up-regulate the expression and uptake activity of GLT-1. Therefore, the present study was undertaken to explore whether Cef can improve the learning and memory deficits of APP/PS1 mice at 7- and 6-month age by up-regulating the expression of GLT-1 and then promoting the glutamate-glutamine cycle by assaying the expression and activity of glutamate synthetase (GS) and the expression of system N glutamine transporter SN1, which are related to the glutamate-glutamine cycle. The learning and memory functions were examined by Novel object recognition and Morris water maze tests. The expressions of GLT-1, GS and SN1 in the hippocampus were assayed with immunohistochemistry and western blot analysis, and the GS activity was assayed with spectrophotometry. It was shown that Cef treatment in doses of 200 mg/kg and 300 mg/kg significantly improved the learning and memory deficits of the APP/PS1 mice and up-regulated the expression of GLT-1. Furthermore, the activity of GS and the expression of SN1 were significantly up-regulated as well after the Cef treatment. The above results suggested that Cef could improve the learning and memory deficits of the APP/PS1 mice in early stage of AD by promoting the glutamate-glutamine cycle. Key words: Ceftriaxone, GLT-1, glutamate-glutamine cycle, APP/PS1 mice

    Time:

    Title: The Relationship Between Physical Activity and Working Memory in Postmenopausal Women: An ERP Study

    Chenglin Zhou
    Shanghai University of Sport, China

    Biography
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    Biography

    Chenglin Zhou
    Shanghai University of Sport, China

    Chenglin Zhou is a professor in the School of Sport Science at the Shanghai University of Sport. In 2016, he was elected to the Yangtze river scholars Distinguished Professor. Chenglin Zhou also serves as the vice chairman of Professional Committee of Sport Psychology, the member of Psychology Teaching Committee, and the member of China Social Neuroscience Committee etc. He is the reviewer of Sport Science, Progress in Psychology, Chinese Sport Medicine, and Journal of Shanghai University of Sport etc. Chenglin Zhou has successfully applied for 18 research projects and published more than 70 papers to date.



    Abstract
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    Abstract

    Chenglin Zhou
    Shanghai University of Sport, China

    Background: Working memory (WM), which refers to the ability to temporarily store and manipulate information that underpins many cognitive processes. It is critical to the daily life and will decline with aging, but can be improved at any time over the lifespan. Therefore, proper interventions on the decline could improve the quality of life of the elderly. The effect of exercise on WM has been a subject of increasing interest over the past few years. Objective: The study aims to determine whether long-term highly physical activity affects WM among postmenopausal women from behavioral and neuroelectric perspectives. Methods: The postmenopausal women were screened by physical tests and grouped into a higher physical activity group (HG; n = 20) and moderate physical activity group (MG; n = 20) according to their physical activity level. They were also required to complete the 1-back task (high workload) and 3-back task (low workload). Results: The behavioral results showed that the HG had quicker and more accurate response in both high and low load conditions compared to the MG. The HG showed increased P3 amplitude than MG in both tasks. The P3 latency in 3-back task was significantly longer than that in 1-back for MG, while there was no significant difference between two load conditions in HG. Conclusion: Our results confirmed that physical activity was positively related to working memory in postmenopausal women and that this positive relationship was associated with the allocation of more attentional resources to increase the efficiency across different memory workloads.

    Time:

    Title: Effects of State Emotions on the Outcome Evaluation Stage of Decision Making in High-anxious Individuals: An ERP Study

    Yingying Wang
    Shanghai University of Sport, China

    Biography
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    Biography

    Yingying Wang
    Shanghai University of Sport, China

    Yingying Wang is currently a Ph.D candidate majoring in sport psychology in Shanghai University of Sport. Yingying Wang has got the approval from China Scholarship Council and become a visiting student in University of Jyvaskyla (JYU) in Finland from January 26, 2018 to January 26, 2019. Her primary research interests are in the areas of sport neuroscience and decision making. She has published in Biological Psychology.



    Abstract
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    Abstract

    Yingying Wang
    Shanghai University of Sport, China

    Background: Human emotions play a powerful role in the decision making process. The influence of emotion on decision making is common in everyday life and has drawn much attention from researchers. According to previous literature, both state emotions (transient responses associated with the current situation) and dispositional emotions (e.g. anxiety) have significant impacts on decision making. However, little is known about their interaction effects on decision making, which is the main interest of the current study. Objective: In this study, to investigate the influence of incidental emotions on decision making in high-anxious individuals, they and the low-anxious individuals were required to perform a monetary gambling task. Methods: Behavioral (the average number of risk-avoidant choices) and electroencephalography (FRN and P3 components) responses were recorded to explore the stages of option assessment and outcome evaluation during decision making, respectively. Incidental emotions were elicited by facial expression pictures presented on the background, which included four conditions (control, neutral, fearful, and happy). Results: The behavioral results showed that there was no significant difference between groups in the average numbers of risk avoidant choices. However, the ERP results showed smaller feedback-related negativity (FRN) amplitudes in high-anxious participants than low-anxious participants in the control, neutral, and fearful conditions, but not in the happy condition, for small outcomes. The P3 amplitudes were larger in high-anxious participants compared to theircounterparts in the fearful and happy conditions, but not in the other conditions. Conclusion: In short, the interaction effects between trait anxiety and facial emotions manifestedon the outcome evaluation stage of decisionmaking.

    Time:

    Title: Ceftriaxone up-Regulates Neuronal Glutamate/Glutamine Transporters in Early Stage of the APP/PS1 Transgenic Mice

    ShuJuan Fan
    Hebei Medical University, China

    Biography
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    Biography

    ShuJuan Fan
    Hebei Medical University, China

    Shujuan Fan is a Doctor in Department of Pathophysiology, Hebei Medical University, China. She graduated from Hebei medical university. At present, She mainly focuses on the fundamental research of the prevention and therapy of Alzheimer’s disease.



    Abstract
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    Abstract

    ShuJuan Fan
    Hebei Medical University, China

    Alzheimer's disease (AD) is characterized by progressive impairment of learning, memory and cognitive functions. Glutamate as neurotransmitter plays an important role in learning, memory and cognition. Excitatory synaptic transmission of glutamatergic neuron requires a continuous release of glutamate from presynaptic terminals. Increasing evidence has shown the down-regulated expression of neuronal glutamine transport (GLnT), vesicular glutamate transporters (VGLUTs) in hippocampal neurons of AD mice. Ceftriaxone (Cef) has been reported to alleviate the cognition deficits of APP/PS1 mice. Therefore, in order to elucidate the mechanism involved in the improvement of Cef for the cognition deficits of APP/PS1 mice, the present study was undertaken to explore whether Cef can up-regulate the expression of GLnT, VGLUTs and metabotropic glutamate receptors 2 and 3 (mGLuR2/3), which are related to the release of glutamate from presynaptic terminals, and whether Cef could impact the levels of Aβ1-40 and Aβ1-42. The learning and memory functions were examined by Novel object recognition and Morris water maze tests. The expressions of GLnT, VGLUTs and mGLuR2/3 in the hippocampus were assayed with immunohistochemistry and western blot analysis. It was shown that Cef treatment in doses of 200 mg/kg and 300 mg/kg significantly improved the learning and memory deficits of the APP/PS1 mice and up-regulated the expression of GLnT, VGLUTs and mGLuR2/3. However, Cef had no effects on the levels of soluble and insoluble Aβ1-40 and Aβ1-42. The above results suggested that Cef could upregulate the expression of proteins associated the releasing of glutamate from neurons, which might contribute to the improvement of Cef for the cognitive deficits of the APP/PS1 mice in early stage of AD. Key words: Ceftriaxone, GLnT, VGLUTs, APP/PS1 mice

    Time:

    Title: A Piloting Study on Visuospatial Attention in Parkinson Disease

    Francesco Terrenzio
    University of Turin, Italy

    Biography
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    Biography

    Francesco Terrenzio
    University of Turin, Italy

    Francesco Terrenzio has obtained his Bachelor’s degree in Psychology at the University of Chieti-Pescara and is currently studying for a Master’s degree in Cognitive Neuroscience at the University of Turin. His research is focused on neurodegenerative diseases, with a strong interest in the Parkinson’s disease. During his internship at the Molinette Neurology department, he is performing a research to explore visuospatial impairment in Parkinson’s patients.



    Abstract
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    Abstract

    Francesco Terrenzio
    University of Turin, Italy

    Parkinson’s disease [PD] is characterized by disorders of visuospatial dysfunction, negatively impacting everyday functioning. Visuospatial difficulties seem to be more prominent in those whose motor symptoms begin on the left body side [LPD] than the right body side [RPD]. The aim of the case report is to assess these potential contributors through performance on a visuospatial line bisection task. Participants included 2 PD patients with motor symptoms asymmetry [LPD, RPD] and 10 normal controls. Visuospatial attention was assessed using a line bisection task, in which participants were asked to mark the middle of 40 horizontal lines. Twenty lines were bisected using the right hand and twenty lines using the left hand. Results show that all participants produced a leftward bisection bias that was greater in the left than in the right hand condition. Both the PD patients produced a significant greater leftward deviation than controls when the task is performed with the right hand, and with the left hand for the LPD when he/she performed the task with the left hand. Conversely, the RPD patient produced a significant greater rightward deviation than controls when he/she performed the task with the left hand. These data are congruent with research in humans supporting the idea that dopamine plays an important role in spatial orienting. Pseudoneglect is viewed as reflecting right hemisphere specialization for processing spatial information, resulting in orienting toward the contralateral hemispace. Our results suggest that visuospatial function in PD could reflect asymmetric dopamine neurotransmission in LPD/RPD.

    Time:

    Title: Inhibition of Drp1 Ameliorates Aβ Toxicity in Alzheimer’s Disease Model

    Dong-Hyung Cho
    Kyung Hee University, South Korea

    Biography
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    Biography

    Dong-Hyung Cho
    Kyung Hee University, South Korea

    Dong-Hyung Cho is an Associate Professor in Graduate School of East-West Medical Science at Kyung Hee Universtiy (South Korea). He obtained PhD at Gwangju Institute of Science and Technology at 2005. He was a post-doctoral fellow in Sanford Burnham Preys Medical Discovery Institute in San Diego, USA. He has focused on mitochondrial dynamics and selective autophagy.



    Abstract
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    Abstract

    Dong-Hyung Cho
    Kyung Hee University, South Korea

    Excessive mitochondrial fission is a prominent early event, and contributes to mitochondrial dysfunction, synaptic failure and neuronal cell death in the progression of Alzheimer’s disease (AD). In the present study, we examine the role of Drp1, a key regulator of mitochondrial fragmentation, in mitochondrial and synaptic dysfunction-induced by Aβ, and AD-like neuropathology and cognitive functions in AD mice. Our results demonstrate that the treatment of a Drp1 inhibitor, Mdivi-1 alleviates mitochondrial fragmentation, loss of mitochondrial membrane potential, ROS production, and ATP reduction in neurons treated with Aβ oligomers. Furthermore, Drp1 inhibition significantly improves learning and memory, synaptic density, and prevents mitochondrial fission, lipid peroxidation, BACE1 expression and A deposition in an AD mouse model. These results provide evidence that Drp1 plays an important role in Aβ-mediated and AD-related neuropathology, and in cognitive function in an AD animal model. Thus, inhibiting excessive Drp1-mediated mitochondrial fission may be an efficient therapeutic avenue for AD.

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