International Conference on
Alzheimer's Disease & Associated Disorders

May 7-9, 2018 | Rome, Italy

Program Schedule

  • Keynote Speaker

    Time:

    Title

    Title: Role of Microbiota Derived Short Chain Fatty Acids in α-Synuclein Aggregation and Seeding

    Giulio Pasinetti
    Icahn School of Medicine, Mount Sinai, USA
    Biography
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    Biography

    Giulio Pasinetti
    Icahn School of Medicine, Mount Sinai, USA

    Dr. Giulio Maria Pasinetti is the Saunders Family Chair and Professor of Neurology at the Icahn School of Medicine at Mount Sinai. He is the Program Director of the Center on Molecular Integrative Neuroresilience. The primary goal of the Center grant is understand the molecular mechanisms and pathophysiology that may be at the basis of stress-induced mood disorders, which are major risk factors for acceleration of age-related Alzheimer’s diseaseand other forms of dementia.Dr. Pasinetti’s Center is currently testingnovel brain bioavailable bioactive “phytodrugs” that have been characterized by the Center in experimental models of disease in translational Alzheimer’s disease preventative trials.



    Abstract
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    Abstract

    Giulio Pasinetti
    Icahn School of Medicine, Mount Sinai, USA

    Objective: To determine whether microbiome derived short chain fatty acid (SCFA) may modulate abnormal α-¬synuclein misfolding and seeding activity of α-synuclein to support the hypothesis of potential novel therapeutic approaches. Background: There is growing evidence from both in vivo and in vitro studies that in many neurodegenerative disorders, including synucleinopathies, cell-to-cell transmission of a pathological, misfolded protein occurs and may be a vehicle for spreading of pathology throughout the brain. We hereby investigate whether microbiota-derived SCFAs may help attenuate the misfolding of α-synuclein and their effects on seeding synucleinopathy. Design/Methods: In vitro aggregation of α-synuclein in the absence or in the presence of SCFAs at a molar ratio of 1:1 or 1:4 α¬-synuclein:SCFA, were monitored by using independent assays: photo-induced cross-linking of unmodified proteins assay, thioflavin-T, fluorescence assay, or electron microscopy. Results: We found that select microbiome-derived SCFAs significantly interfere with α-synuclein aggregation in independent in vitro assays. Conclusions: Select microbiome-derived SCFAs may help protect against diverse synucleinopathies by converting dietary fibers into biologically available SCFAs which significantly interfere with aggregation of disease-specific α¬synuclein into toxic aggregates. Ongoing cell-based systems, which detect levels of α-synuclein by florescent FRET signaling, will clarify the impact of this anti-aggregation activity of SCFAs on interference of α-synuclein seeding activity that is critical for the propagation of α-synuclein mediated pathologies. This data will help to clarify distinct α-synuclein seeding activity from α-synuclein isolated from post-mortem brain samples of patients with Parkinson’s disease, multiple systemic atrophies, and other synucleinopathies, leading to novel therapeutic approaches.

    Keynote Speaker

    Time:

    Title

    Title: Self-reported Cognitive Decline and its Role in Early Detection of Dementias

    Simona F. Sacuiu
    Gothenburg University, Sweden
    Biography
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    Biography

    Simona F. Sacuiu
    Gothenburg University, Sweden

    Simona F Sacuiuis a psychiatrist with a strong curriculum in epidemiologic study of mild cognitive impairment (MCI). She leads the MCI group within the EpiNep Research Group at the Institute of Neuroscience and Physiology, University of Gothenburg, Sweden. The MCI groupstudies MCI with affective symtoms and its long-term prognosis. She has been part of diverse collaborations during the past 15 years at the University of Gothenburg within the Swedish Brain Power as well as internationally within EURODEM-DESCRIPA, the Alzheimer’s disease Neuroimaging Initiative. She supports the burgeoning Alzheimer’s research in her native country Romania.



    Abstract
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    Abstract

    Simona F. Sacuiu
    Gothenburg University, Sweden

    Self-reported cognitive decline (SCD) is the usual trigger for dementia investigation in primary care. Although there is an increased requirement for diagnosis of dementia at the primary care level it is unknown what is the sensitivity and specificity of SCD in early stages of dementia. The association between subjective cognitive symptoms and the development of dementia seem to be modulated by thepresence of mood disorders and self-awareness of cognitive changes. The self-awareness diminishes in later stages of dementia. This could partly explain that SCD are not always correlated with cognitive screening tests results. Some attention has been drawn lately to associations found between SCD and pathologic biomarkers of dementia, especially of dementia due to Alzheimer’s disease. Taking into consideration the interactions betweenthese factors and the risk to develop dementia may add diagnostic value to self-reports in dementia work-up. The proposed plenary session will address largely unclear issues related to early diagnosis and prediction of dementiawith focus on SCD using results from ongoing epidemiologic longitudinal studies of aging and dementia in Gothenburg, Sweden, the well-known H70 studies, in relation to the existant literature.

    Sessions:
    Animal Models for Alzheimer and Neurodegeneration

    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

    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.

    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: Dementia with Lewy Bodies Psychopathology and Evidence Based Management

    Vinodkumar Gangolli
    McMaster University, Canada

    Biography
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    Biography

    Vinodkumar Gangolli
    McMaster University, Canada

    Dr. Vinodkumar Gangolli is a Fellow of the Royal College of Physicians and Surgeons of Canada, a Member of the Royal College of Psychiatrists, London, England, and is Board certified in Psychiatry and Geriatric Psychiatry by the American Board of Psychiatry and Neurology, Chicago, USA. He holds the post of Assistant Clinical Professor of Psychiatry (adjunct), in the Department of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, Ontario, Canada. He is also a Consultant Psychiatrist in the Department of Psychiatry, Grand River Hospital Corp., Kitchener, Ontario, Canada and Dean of Academics at Masina Hospital, Byculla, Mumbai, India. He is a member of WHO ICD-11 Consultation group of Mental and Behavioral Disorders in Older Adults, Geneva, Switzerland.



    Abstract
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    Abstract

    Vinodkumar Gangolli
    McMaster University, Canada

    Dementia with Lewy bodies is an under-recognized disease; it is responsible for up to 20 % of all dementia cases. Accurate diagnosis is essential because the management of dementia with Lewy bodies is more complex. Alpha-synuclein, the pathological protein responsible for dementia with Lewy bodies (and Parkinson’s disease), produces symptoms in multiple domains. A comprehensive treatment strategy can be achieved by treating core clinical features such as cognitive, neuropsychiatric, movement, autonomic, and sleep categories. Invariably the treatment of one set of symptoms can cause complications in other symptom domains, but a comprehensive treatment program can greatly improve the patient’ s quality of life, but does not alter the progression of disease. Cholinesterase inhibitors are effective for cognitive and neuropsychiatric symptoms; Special care needs to be taken to avoid potentially fatal idiopathic reactions to neuroleptic medications; these should be used for short periods only when absolutely necessary and when alternative treatments have failed. Pimavanserin, a selective serotonin 5-HT2A inverse agonist, holds promise as an alternative therapy for synuclein-associated psychosis. Levodopa/carbidopa treatment of Parkinsonism is often limited by dopa-induced exacerbations of neuropsychiatric and cognitive symptoms. Autonomic symptoms are under-recognized complications of synucleinopathy. Constipation, urinary symptoms and postural hypotension respond to standard medications. Rapid eye movement sleep behavior disorder is highly specific (98 %)to the synucleinopathies. Non-pharmacological treatments, melatonin and clonazepam are all effective.

    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.

    Sessions:
    Memory Disorders & Neurologic Problems & Neuropsychology & Neuropathology

    Time:

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

    Anastasios Georgakopoulos
    Icahn School of Medicine at Mount Sinai, USA

    Biography
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    Biography

    Anastasios Georgakopoulos
    Icahn School of Medicine at Mount Sinai, USA

    He 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

    Anastasios 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: Nose to Brain Delivery of Formulation by Design (FbD)- Enabled Quercetin Nanocarriers for Neurocognitive Disorders

    Charan Singh
    Panjab University, India

    Biography
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    Biography

    Charan Singh
    Panjab University, India



    Abstract
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    Abstract

    Charan Singh
    Panjab University, India

    In the present study, Formulation by Design (FbD) enabled lipidic nanostructured system (NLCs) were formulated for quercetin. They were evaluated for their efficiency in nose-to-brain targeting and biodistribution in a suitable animal model after intranasal delivery. Further, particles size characterization revealed uniform shape with size less than 200 nm. Stability studies indicated refrigeration found to be the preferred storage condition. The intranasal delivery of quercetin nanoconstructs resulted in over 8 folds increase in relative brain vis-a-vis pure drug. The brain distribution studies of nanoconstructs exhibited significantly higher Cmax (825.3±76 vs. 611.23 ±15 µg per gram of brain tissue), delayed Tmax (4±1 vs.2± 0.5 h), prolonged T1/2 (64.1±12 vs.12.62±1 h), MRT (36.80±2 vs. 6.93±0.5 h) and enhanced AUC0-∞ (30914.33±113 vs. 3849.40±20 µg h/L) vis-a-vis pure quercetin. Moreover, biodistribution studies revealed lower quercetin concentration in the in non targeted tissues following intranasal delivery of nanoconstructs. Hence, the current investigation demonstrates the potential of nano-antioxidant as a potent therapeutic intervention for HIV associated neurocognitive disorders with improved biopharmaceutical attributes.

    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. His 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.

  • Sessions:
    Alzheimers Disease & Dementia

    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



    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: 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: Early and Persistent O-GlcNAc Protein Modification in the Streptozotocin Model of Alzheimer’sDisease

    Carlos-Alberto Goncalves
    Federal University of Rio Grande do Sul, Brazil

    Biography
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    Biography

    Carlos-Alberto Goncalves
    Federal University of Rio Grande do Sul, Brazil

    Carlos-Alberto Gonçalves is a medical doctor from Catholic University of Pelotas (Brazil, 1985), MSc and PhD in biochemistry from Federal University of Rio Grande do Sul (Brazil, 1992) and post-doctoral in neurochemistry from the University of Newcastle (Australia, 1995). He is full professor at Federal University of Rio Grande do Sul, working on programs of biochemistry and neuroscience. He is fellow researcher from National Council for Development of Science and Technology (CNPq) and honorary member of Cuban Society of Neuroimmunology. His basic and applied neurochemistry research focusing in: Activity, expression and secretion of S100B, a calcium-binding protein and Markers of glial activation in neurodegenerative diseases, particularly Alzheimer‘s disease.



    Abstract
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    Abstract

    Carlos-Alberto Goncalves
    Federal University of Rio Grande do Sul, Brazil

    O-GlcNActransferase (OGT), an enzyme highly expressed in brain tissue, catalyzes the addition of N-acetylglucosamine (GlcNAc) to hydroxyl residues of serine and threonine of proteins. Brain protein O-GlcNAcylation is diminished in Alzheimer’s disease (AD), and OGT targets include proteins of the insulin-signaling pathway (e.g., insulin receptor susbtrate-1, IRS-1). We hypothesized that ICV streptozotocin (STZ) also affects O-GlcNAc protein modification. We investigated hippocampal metabolic changes in Wistar rats, particularly OGT levels and insulin resistance, as well as related astroglial activities, immediately after ICV STZ administration (first week) and later on (fourth week). We found an early (at one week) and persistent (at fourth week) decrease in OGT in the STZ model of AD, characterized by a spatial cognitive deficit. Consistent with this observation, we observed a decrease in protein O-GlnNAc modification at both times. Increased phosphorylation at serine-307 of IRS-1, which is related to insulin resistance, was observed on the fourth week. The decrease in OGT and consequent protein O-GlnNAc modifications appear to precede the decrease in glucose uptake and increment of the glyoxalase system observed in the hippocampus. Changes in glial fibrillary acidic protein and S100B in the hippocampus, as well as the alterations in cerebrospinal fluid S100B, confirm the astrogliosis. Moreover, we found signs of astroglial dysfunction, which are likely implicated in the neurodegenerative cascade triggered in this model. Together, these data contribute to the understanding of neurochemical changes in the STZ model of AD, and may explain the decreases in protein O-GlcNAc levels and insulin resistance observed in AD.

    Time:

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

    Beka Solomon
    Tel Aviv University, Isreal

    Biography
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    Biography

    Beka Solomon
    Tel Aviv University, Isreal

    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, Isreal

    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: 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: 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.

    Sessions:
    Diagnosis & Prevention & Behavioural & Psychiatric Symptoms

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

    Robert Norman
    Nova SouthEastern University, USA

    Biography
    χ

    Biography

    Robert Norman
    Nova SouthEastern University, USA



    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

    Time:

    Title: Clinical Correlates with Functional Neuroimaging: From Case Reports to Clinical Researches

    Kenichi Meguro
    Tohoku University, Japan

    Biography
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    Biography

    Kenichi Meguro
    Tohoku University, Japan

    Kenichi Meguro is a Professor in Geriatric Behavioral Neurology, Tohoku University,Japan.He is a director of Tajiri Skip Center. He Graduated from Tohoku University Graduate School of Medicine. He is a Executive Committee of INA and ASAD, Councilor of Japanese Society of Cognitive Neuroscience, Higher Brain Dysfunction, Neuropsychology Association, Psychogeriatric Association, and Society for Dementia Research.



    Abstract
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    Abstract

    Kenichi Meguro
    Tohoku University, Japan

    An approach based on behavioral neurology is important for better understanding of 1) behavioral abnormality, 2) neuronal network, and 3) rehabilitation for patients with cognitive impairment. Mainly, neurological background of human behavior is consisted of three parts, i.e., the hierarchical axis (“old brain” vs “new brain”), the left-right axis (“language brain” vs “non- language brain”), and the anterior-posterior axis (“behavioral brain” vs “cognitive brain”). 1) Behavioral Abnormality A case with right basal ganglia infarction is reported, who disclosed hyperactivity and confabulation. We found right basal ganglia infarction (MRI) and decreased blood flow to the right frontal lobe (SPECT). After the physician in charge provided an explanation, the patient began to be conscious about her disease and agreed to undergo drug treatment. 2) Neuronal Network A case with left thalamic infarction is reported, who developed difficulty finding words and used many pronouns in her communication. MRI showed infarction in the left thalamus and SPECT revealed decreased CBF in the bilateral anterior cingulate blood flow. The fronto-subcortical network and the Yakovlev and Papez networks are considered to understand the symptoms. 3) Rehabilitation A case with vascular MCI is reported, who took a longer time to learn the exercises with decreased working memory capacity. Working memory maintenance promotes long-term memory information. The anterior cingulate cortex plays an important role in dual-task situations. Dual-task during unfamiliar movement could be stressed the working memory capacity. The cingulo-frontal network may be partially blocked by the deep white matter lesions in this case.

    Sessions:
    Poster Session

    Time:

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

    WenBin Li
    Hebei Medical University, China

    Biography
    χ

    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: Neuroprotective Potential of Galantamine along with Coenzyme Q10 and Taurine against Aβ (1-42) Induced Cognitive Dysfunction: Involvement of Mitochondrial Dysfunction, Oxidative Damage, Neuroinflammation and Histopathological Alterations

    Arti Singh
    Panjab University, India

    Biography
    χ

    Biography

    Arti Singh
    Panjab University, India



    Abstract
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    Abstract

    Arti Singh
    Panjab University, India

    Taurine, 2-aminoethanesulfonic acid, acts as a neuromodulator, prevent mitochondrial dysfunction, apoptosis and oxidative stress. Coenzyme Q 10 (CoQ10), a lipophilic, endogenous, vitamin-like antioxidant compound. Galantamine, acetylcholinesterase inhibitors (AChEIs), is a novel treatment for AD and modulates nicotinic acetylcholine receptors (nAChRs). We aimed to evaluate the neuroprotective potential of taurine and CoQ10 along with galantamine in A (1-42) induced cognitive dysfunction in rats. Intrahippocampal (i.h.) Aβ (1-42) (1µg/µl; 4µl/site) were administered, followed by drug treatment with taurine (25 and 50 mg/kg), CoQ10 (10 and 20 mg/kg), galantamine (2 mg/kg) and their combinations for a period of 21 days. Various neurobehavioral parameters followed by biochemical, AChEs level, mitochondrial enzyme complex level (I-IV), TNF-α level and histopathological alterations were assessed. Aβ (1-42) administration significantly impaired cognitive performance in Morris water maze (MWM) test, causes oxidative stress, raised AChEs level, neuroinflammation, mitochondrial dysfunction and histopathological alterations as compared to the sham treatment. Treatment with taurine (25 and 50 mg/kg), CoQ10 (10 and 20 mg/kg) and galantamine (2 mg/kg) improved cognitive performance in MWM test, reduced AChEs activity, neuroinflammation, oxidative damage, TNF-α level, restored mitochondrial respiratory enzyme complex (I-IV) activities and histopathological alterations as compared to Aβ (1-42) treated animals. Further, combinations of taurine (25 and 50 mg/kg) and CoQ10 (10 and 20 mg/kg) and their interaction with galantamine (2 mg/kg) significantly (P<0.05) modulate the neuroprotective potential of galantamine (2 mg/kg) as compared to their effect per se in Aβ (1-42) treated animals. The present study suggests the neuropotentiating effect of taurine and CoQ10 on galantamine in Aβ (1-42) treated animals. Keywords: Alzheimer’s disease, A (1-42), CoQ10, taurine, galantamine, mitochondrial dysfunction, oxidative stress, neuroinflammation.

    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
    χ

    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

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