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Brainflammation: The Role of the Innate Immune System in CNS Disorders

Brainflammation: The Role of the Innate Immune System in CNS Disorders

Tuesday, December 6, 2011

The New York Academy of Sciences

Neuroinflammation has been implicated in nearly every disorder of the CNS. As the resident innate immune cells of the CNS, microglia are the vanguard in host defense and in tissue repair. Their constant surveillance of the CNS enables them to rapidly respond to invading pathogens as well as mechanical or chemical injury. However, a growing body of evidence indicates that chronic or maladaptive activation of these very same cells plays a critical role in a variety of CNS disorders (including autism, psychiatric disorders, epilepsy, and neurodegenerative diseases such as AD, PD, ALS, and MS). Furthermore, recent work suggests that peripheral monocytes (another component of the innate immune system) may also become activated and then recruited to the CNS where they contribute to the regulation of neuroinflammation and the course of such disorders. These two cell populations, separated by the blood brain barrier and time, may therefore provide a key link between peripheral and central inflammatory processes. This symposium gathers experts on microglia/monocyte biology to discuss the role of the innate immune system in neurological disorders, what insights can be learned about their biology from their dysfunction in various disease contexts, and possible therapeutic interventions.

Networking reception to follow.

Registration Pricing

Student / Postdoc / Fellow Member$10
Student / Postdoc / Fellow Nonmember$40
Nonmember Academic$60
Nonmember Not for Profit$60
Nonmember Corporate$80


Presented by

  • New York Academy of Sciences


* Presentation times are subject to change.

Tuesday, December 6, 2011

8:30 AM

Registration & Continental Breakfast

9:00 AM

Sean Pintchovski, PhD and Roland Staal, PhD, Lundbeck Research USA

9:15 AM

The Impact of Systemic Inflammation on the Healthy and Diseased Brain
V. Hugh Perry, DPhil, University of Southampton, UK

10:00 AM

Microglia and Monocytes: Kith or Kin?
Richard Ransohoff, MD, Lerner Research Institute

10:45 AM

Coffee Break

11:15 AM

Microglia / Macrophage Responses during Chronological Aging
Dave Morgan, PhD, University of South Florida

12:00 PM

CD45 and CD40 Modulation of Microglial Activation: Implications for Alzheimer's and HIV Associated Dementias
Jun Tan, MD, PhD, University of South Florida College of Medicine

12:45 PM

Lunch Break

1:30 PM

Dysfunctional Microglia in the Pathogenic Mechanisms Underlying Autism
Carlos A. Pardo-Villamizar, PhD, Johns Hopkins University School of Medicine

2:15 PM

An Imbalanced Neuro-immuno-endocrine Set Point as a Cause for Major Mental Disorders
Hemmo A. Drexhage, MD, PhD, Erasmus Medical Center

3:00 PM

Coffee Break

3:30 PM

Seizing Opportunities in Microglial Biology for Epilepsy
Annamaria Vezzani, PhD, Mario Negri Institute for Pharmacological Research

4:15 PM

Microglia, What a (Neuropathic) Pain!
Ru-Rong Ji, PhD, Harvard University and Brigham & Women's Hospital

5:00 PM

Networking Reception

6:00 PM




Robert Martone

Covance Biomarker Center of Excellence

Robert Martone is Neuroscience Therapeutic Area Lead for the Covance Biomarker Center of Excellence. He has extensive experience in the pharmaceutical industry leading neuroscience drug discovery and technology teams through all phases of discovery from target identification through clinical trials with expertise in both small molecule and protein therapeutics. He also has several years of academic research experience  in molecular neurobiology, with a focus on the molecular genetics of familial neuropathies, and CNS tumor biomarker development.

Sean Pintchovski, PhD

Lundbeck Research USA

Dr. Pintchovski earned a BS with Honors from the California Institute of Technology and a PhD in Neuroscience from the University of California, San Francisco while working at the Gladstone Institute of Neurological Disease and studying the regulation of neuronal gene expression underlying memory and cognition. After completing a postdoctoral fellowship at Elan Pharmaceuticals, where he worked to further elucidate key processes that contribute to cognitive decline in Alzheimer's disease, Dr. Pintchovski joined the Neuroinflammation Department at Lundbeck as a research scientist in early 2010. At Lundbeck his efforts have focused on applying a range of cutting edge techniques, including ex vivo FACS, to uncover how dysregulation of the immune system contributes to the pathogenesis of various neurodegenerative and psychiatric conditions. Dr. Pintchovski is driven by the desire to translate such fundamental discoveries into novel therapeutic approaches that will address the medical and social challenges posed by these devastating diseases.

Roland Staal, PhD

Lundbeck Research USA

Roland Staal received his PhD in Pharmacology from the University of Medicine and Dentistry of NJ with a focus on in vivo models of dopaminergic neurodegeneration, including amphetamines and MPTP, an animal model of Parkinson's disease. He did his post-doctoral studies at Columbia University, where he studied the function of alpha-synuclein as well as its role in sensitizing mice to the Parkinsonian neurotoxin MPTP. He then joined Wyeth Research's department of neurodegeneration, studying protein mis-folding and potential therapeutic interventions including aggregation inhibitors and immunotherapies for both Parkinson's and Alzheimer's disease. He then joined Lundbeck Research, where he was instrumental in establishing the Neuroinflammation biology unit. The unit works with various technologies including flow cytometry, cell sorting, ELISAs and Cellomics to evaluate various markers and outcomes of Neuroinflammation in in vivo models as well as cell lines and primary neuronal and microglial cultures. His current focus is on targeting neuroinflammatory aspects of CNS diseases, in particular, neuronal–microglial communication.

Jennifer Henry, PhD

The New York Academy of Sciences


Hemmo A. Drexhage, MD, PhD

Erasmus Medical Center

Dr. Hemmo A. Drexhage is professor in Medical Immunology at the ErasmusMC (Rotterdam). He graduated from medical school in 1974 (Amsterdam), defended his immunology PhD thesis in 1977 (Amsterdam) and studied immunology/medical immunology with Brigid Balfour/John Humphrey (Mill Hill) and Ivan Roitt and Deborah Doniach (Middlesex Hospital) in London from 1976–1981 (on exchange grants of the Royal Dutch and English Societies of Science). His subject of studies has ever since been focussed on the clinical picture and immune diagnosis of autoimmune diseases of endocrine glands (thyroid, islets of Langerhans, adrenal, ovary, pituitary) and the initiating role of aberrant dendritic cells and macrophages in thepathogenesis of these diseases. The higher prevalence of endocrine autoimmunities in severe mood disorders sparkled in 1996 his interest into studies on the role of immune cells in bipolar disorder, major depressive disorder, post partum psychosis and schizophrenia. He has published over 350 articles/book chapters on these subjects and supervised more than 30 PhD students.

Ru-Rong Ji, PhD

Harvard University and Brigham & Women's Hospital

Ru-Rong Ji received his PhD degree in Neurobiology at Shanghai Institute of Physiology, Chinese Academy of Sciences. He had postdoctoral trainings in Peking University, Karolinska Institute, and Harvard Medical School. Currently he is an associate professor at Brigham and Women's Hospital, Harvard Medical School. He is also director of Sensory Plasticity Laboratory and associate director of the Pain Research Center. He has been working on spinal cord mechanisms of chronic pain for 20 years. His work has demonstrated important roles of glial cells (eg., microglia), MAP kinase signaling pathways, and cytokines/chemokines in the control of neuropathic pain. His recent work has also revealed important role of pro-resolution lipid mediators in the resolution of inflammation and pain. Dr. Ji has published more than one hundred papers on chronic pain mechanisms and treatments.

Dave Morgan, PhD

University of South Florida

Dave Morgan is Chief Executive Officer/Director of the USF Health Byrd Alzheimer Institute, Distinguished Professor of Molecular Pharmacology and Physiology, and Director of Neuroscience Research for the College of Medicine and at the University of South Florida. Dr. Morgan’s research interests are aging and brain function, focusing on drugs to treat Alzheimer’s dementia. Morgan participated in the development of a transgenic mouse model of Alzheimer's disease (APP+PS1). His work focuses largely on the neuro-immune interactions associated with the Alzheimer phenotype, and the role of astrocytes and microglia in the disease process. He is presently testing anti-amyloid immunotherapy and gene therapy to treat the Alzheimer-like changes in transgenic mouse models of the disease. This work is supported by multiple grants from the NIH, private foundations and contracts from industrial partners. Morgan regularly sits on review panels for NIH and other agencies evaluating grants to develop new drugs to treat Alzheimer's and other neurodegenerative disorders.

Carlos A. Pardo-Villamizar, MD

Johns Hopkins University School of Medicine

Dr. Pardo is an Associate Professor of Neurology and clinician-scientist at Johns Hopkins University School of Medicine, Department of Neurology (Division of Neuroimmunology and Neuroinfectious Disorders) and Pathology (Neuropathology) in Baltimore, Maryland. He is the principal investigator of the Neuroimmunopathology Laboratory, member of the HIV Neurosciences Research Group and clinical neurologist at the Multiple Sclerosis and Transverse Myelitis Centers at Johns Hopkins Hospital. Dr. Pardo's research interest and laboratory work focuses on studies of the 1) Immunopathological and molecular mechanisms of associated with neuroimmune disorders such as multiple sclerosis, neuroAIDS as well as epilepsy and autism, 2) the role of cytokines and chemokines in neurobiological processes and pathogenic mechanisms in neurological disorders, 3) Studies of biomarkers of neuroimunological disease in cerebrospinal fluid and blood and 4) Animal models of neuroimmunological disorders. Dr. Pardo's interest on autism centers on the role of neuroimmune factors and neuroglia in the pathogenesis of this neurodevelopmental disorder. His laboratory has contributed to the study of the role of microglia activation in the cerebral cortex and the function of cytokines and chemokines as factors involved in neurobiological processes associated with disturbances of developmental and neurobehavioral trajectories that characterize autism. His laboratory is also working on the identification of CSF and blood biomarkers that may facilitate a better understanding of pathogenesis and phenotypic characterization of autism.

V. Hugh Perry, DPhil

University of Southampton, UK

Hugh Perry obtained his first degree at the University of Oxford where he completed his DPhil in neuroscience in 1977. He remained at the University of Oxford and was appointed to a Locke Fellow of the Royal Society and then a Wellcome Trust Senior Research Fellow. He was appointed Professor in Experimental Neuropathology (1996). In 1998 he moved to the University of Southampton to take up his current post. His research interests are in the field of interactions between the immune system and nervous system. He has published more than 275 peer-reviewed papers. He has sat on research advisory and funding panels for the Medical Research Council, and a number of biomedical charities including the Multiple Sclerosis Society, International Spinal Research Trust and Motor Neuron Disease Association: he chaired the Cellular and Molecular Neuroscience panel of the Wellcome Trust 2004–2007. He has acted as a consultant for biotechnology and pharmaceutical companies in the area of neuroinflammation and neurodegenerative disease. He was elected a Fellow of the Academy of Medical Sciences (2005), is Deputy Chair of the Nuffield Council on Bioethics. He has been appointed to Chair of the Medical Research Council Neuroscience and Mental Health Board from 1st April 2012.

Richard Ransohoff, MD

Lerner Research Institute

Richard M. Ransohoff serves at the Cleveland Clinic as Director of the Neuroinflammation Research Center in the Department of Neurosciences of the Lerner Research Institute; Professor of Molecular Medicine at the Cleveland Clinic Lerner College of Medicine; and Staff Neurologist in the Mellen Center for MS Treatment and Research.

Among his many awards are a Physician's Research Training Award from the American Cancer Society (1984–86); a Clinical Investigator Development Award from the National Institutes of Health (NIH; 1988–1993); the Cleveland Clinic Lerner Research Institute's Award for Excellence in Science in 2006; the Cleveland Clinic's Scientific Achievement Award in Basic Science 2009. He was invited to give the F. E. Bennett Memorial Lecture to the American Neurological Association in 2009. He has been cited from 1996 through the present in "Best Doctors in America" for his expertise in the clinical care of patients with multiple sclerosis (MS).

Dr. Ransohoff serves as regular member on study sections of the NIH and NMSS (as Chair) and is currently a regular member of the CMBG Study Section. He has served on the Editorial Boards of The Journal of Immunology, (2002–2005 as Section Editor) Trends in Immunology, the Journal of Neuroimmunology; Nature Reviews Immunology, and Neurology (Associate Editor).

Dr. Ransohoff's research focuses on the functions of chemokines and chemokine receptors in development, cell biology and pathology of the nervous system. With a longstanding interest in the mechanisms of action of interferon-beta. Dr. Ransohoff has received continuous research support from the NIH and the NMSS for more than 20 years. In Entrez/PubMed, he lists more than 275 articles of which more than 215 are peer-reviewed scientific reports. He has written numerous book chapters, and edited five books.

Dr. Ransohoff is a member of the American Academy of Neurology, the American Neurological Association, and the American Association of Physicians and is a Fellow of the American Association for the Advancement of Science.

Jun Tan, MD, PhD

University of South Florida College of Medicine

In 1983, Dr. Jun Tan received his Bachelors of Medicine at the Third Medical University in Chongqing, China. He went on to earn his Masters of Science in human genetics at Fudan University, Shanghai in 1989. Three years later, he completed his Doctoral Degree at the Third Medical University/Fudan University. Following, he was promoted to both full Professor and Chief of the Department of Molecular Genetics from 1990 to 1994 at the Third Medical University in Chongqing, China. He completed postdoctoral studies in 1996 at the Department of Human Genetics/Immunology at the University of Michigan, Ann Arbor. Dr. Tan then completed his research fellowship in 1998 at H. Lee Moffitt Cancer & Research Institute in Tampa, Florida. Upon completion, he became Assistant Professor of Psychiatry and Microbiology & Immunology at the University of South Florida (USF) in 1998 and Associate Professor 2004. In 2007, Dr. Tan was named the Robert A. Silver Endowed Chair in Developmental Neurobiology and currently directs the Developmental Neurobiology Laboratory at the Silver Child Development Center, USF Department of Psychiatry. Dr. Tan has published over 100 scientific papers, several of them in journals such as Science, Nature Neuroscience, Nature Medicine, EMBO J, PNAS, Journal of Neuroscience, Journal of Immunology, JBC, PloS One, Neurobiology of Disease, and The European Journal of Immunology. Based on these works, Dr. Tan is the recipient of a number of federal grants as PI, including NIH/NINDS (R01/2004), NIH/NIA (P01/2006), NIH/NIA (R01/2009), NIH/NIMH (R21/2007/2010), NIH/NIA (R21/2010) and NIH/NIA (STTR/SBIR/2006/2008/2009). In addition, he also receives funding from the James A. Haley VA Medical Center (2009), the Alzheimer's Association (2004), as well as the Johnny Byrd Alzheimer Center & Institute (2005/2006), and The Institute for the Study of Aging (ISOA/2006).

Annamaria Vezzani, PhD

Mario Negri Institute for Pharmacological Research

Annamaria Vezzani, PhD degree in Neuropharmacology in Milano at the Mario Negri Inst for Pharmacol Res (IRFMN). She spent her post-doctoral period at the Univ of Maryland in Baltimore working in experimental models of epilepsy. Additional post-doctoral periods were done at the Univ of Stockholm and at the Karolinska Institute. She was on sabbatical at the Albert Einstein College of Medicine in 2002 in the laboratory of Developmental Epilepsy.

The present research is on the functional role of neuroactive peptides and inflammatory mediators in the modulation of seizures and in the mechanisms of pharmacoresistance. Since 1997 she is Head of the Laboratory of Experimental Neurology in the Department of Neuroscience at the IRFMN.

Dr. Vezzani is member of the Editorial Board of Epilepsy Currents, Epilepsy Research, Epilepsy and Treatments and Neuroscience and Associate Editor of Basic Science for Epilepsia. She has been appointed (2006–2009) of the Chair of the Commission on Neurobiology of International League Against Epilepsy promoting initiatives for improving translational research in epilepsy. She received the Research Recognition Award for translational research in 2009 by the American Epilepsy Society.


For sponsorship opportunities please contact Carmen McCaffery at or 212.298.8642.

Presented by

  • New York Academy of Sciences

Grant Support

This activity is supported by an educational donation provided by Amgen.

Academy Friends

Bristol-Myers Squibb


Lundbeck Research USA

Promotional Partners

Alzheimer Research Forum

Dana Foundation


The Impact of Systemic Inflammation on the Healthy and Diseased Brain
V. Hugh Perry, DPhil, University of Southampton

The resident macrophages of the brain, the microglia, are observed to be morphologically activated and increase in number during the progression of many chronic neurodegenerative diseases. Observational studies in human postmortem material and studies in animal models seek to define the contribution that this innate immune response makes to the pathogenesis and rate of progression of these diseases. It is well recognized that age is a significant risk factor for diseases such as Alzheimer's disease and Parkinson's diseases and that elderly people commonly have systemic co-morbidities that give rise to systemic inflammation. There is a growing body of evidence to show that systemic infection and inflammation impacts on the progression of chronic neurodegeneration in animal models and that this involves the switching of the microglia phenotype to an aggressive tissue damaging phenotype by the systemic inflammation. Clinical studies in patients with Alzheimer's disease show that chronic systemic inflammation and acute infections are associated with accelerated cognitive decline and exacerbation of the symptoms of sickness. These findings offer new routes to therapeutic interventions to improve the quality of life of those suffering from chronic neurodegenerative disease.

Microglia and Monocytes: Kith or Kin?
Richard Ransohoff, MD, Lerner Research Institute, Cleveland Clinic

Microglia are the resident mononuclear phagocytes (MNP) of the central nervous system (CNS). In the healthy brain, parenchymal microglia exhibit are pressed phenotype, maintained by soluble and membrane-associated inhibitory factors of adjacent neurons and astrocytes, and contingent as well upon the blood-brain barrier's exclusion of plasma proteins. Microglial processes are constitutively motile, monitoring the local microenvironment and palpate synapses. In response to disturbance of CNS homeostasis, microglia undergo morphological and phenotypic changes collectively termed 'activation'. Effector functions of activated microglia are enormously diverse and can either enable or impede CNS recovery, dependent on context. Often, CNS disorders featuring microglial activation are also accompanied by accumulation of blood-derived monocytes in the parenchymal tissues. Both microglia and monocytes give rise to macrophages. Several lines of evidence indicate functional differences between monocyte-derived macrophages as compared with those differentiated from microglia. However, no immunohistochemical markers distinguish monocyte-derived macrophages from resident microglial macrophages. Novel murine genetic models discriminate between resident microglia and infiltrating monocytes, both in the healthy brain and during autoimmune inflammation. Understanding the differential and context-depending roles of hematogenous as compared with brain-derived macrophages will add a new dimension of refinement to therapeutic strategies that target neuroinflammation.

Microglia / Macrophage Responses During Chronological Aging
Dave Morgan, PhD, University of South Florida

Microglial activation in the brain is thought to confer either beneficial or detrimental impacts on the nervous system depending upon the context and type of activation. Most studies of microglia activation in response to various stimuli use either young mice or cells in culture. We have found that the microglial response to activating stimuli in mouse brain differs as a function of mouse age. Moreover, the classical and alternative forms of activation seem to respond to age and antibody therapy in opposite directions. A still unanswered question is the degree to which circulating monocytes can infiltrate the immune system. We find that in brain that is perturbed by the presence of amyloid deposits that sufficient circulating monocytes enter the brain to supply it with a potentially therapeutic gene (neprilysin). Moreover, we find that age appears to increase the extent of monocyte infiltration in both normal as well as mice with amyloid deposits. These results caution that data obtained in young mice may not translate effectively to aged human brain.

CD45 and CD40 Modulation of Microglial Activation: Implications for Alzheimer's and HIV Associated Dementias
Jun Tan, MD, PhD, University of South Florida College of Medicine

Deposition of amyloid-β peptide (Aβ) as β-amyloid plaques in the setting of microgliosis is a defining pathological hallmark of Alzheimer's disease (AD). However, reactive microglia ultimately fail to clear Aβ in brains of AD patients and in mouse models of the disease. It has even been suggested that chronic microglial immune responses contribute to AD pathogenesis by promoting Aβ plaque formation, but the molecular mechanisms underlying this deleterious response have remained elusive. The main focus of our research has been on the role of the CD40–CD40 ligand (CD40L) interactions in regulation of microglia for the treatment of neurodegenerative disease. Over the past years, we discovered that the CD40–CD40L interaction plays a critical role in abnormal amyloid β (Aβ)-induced microglial activation. We have investigated the role of CD45, a membrane-bound protein–tyrosine phosphatase (PTP), in negative regulation of this pathway. The latter work has suggested that triggering CD45 is beneficial because it blocks a very early step in the development of AD. Most recently, we have shown that transgenic mice overproducing Aβ, but deficient in CD45 (PSAPP/CD45−/− mice), faithfully recapitulate AD neuropathology. Specifically, we found: increased abundance of cerebral intra- and extracellular soluble oligomeric and insoluble Aβ, decreased plasma soluble Aβ, increased abundance of microglial neurotoxic cytokines TNF-α and IL-1β, and neuronal loss in PSAPP/CD45−/− mice compared to CD45 sufficient PSAPP littermates. Upon CD45 ablation, in vitro and in vivo studies demonstrate an anti-Aβ phagocytic but pro-inflammatory microglial phenotype. This form of microglial activation occurs with elevated Aβ oligomers and neural injury and loss as determined by decreased ratio of anti-apoptotic Bcl-xL to pro-apoptotic Bax, increased activated caspase-3, mitochondrial dysfunction, and loss of cortical neurons in PSAPP/CD45−/− mice. These data show that deficiency in CD45 activity leads to brain accumulation of neurotoxic Aβ oligomers, and validate CD45-mediated microglial clearance of oligomeric Aβ as a novel AD therapeutic target.
As an extension of this work in a related neurodegenerative disease, HIV associated cognitive disorders (HAND), we investigated the possible role of CD45 in microglial responsiveness to HIV-1 Tat protein. We BV2 microglia when treated with phen and HIV-1 Tat protein (100 nm) become activated in a synergistic pro-inflammatory manner as supported by TNF-&alpha and IL-1β release, both of which were dependent on p44/42 MAPK pathway activation. Stimulation of microglial CD45 by anti-CD45 antibody markedly inhibits these Tat or Tat/phen effects via inhibition of p44/42 MAPK, suggesting CD45 negatively regulates Tat mediated microglial activation. As a validation of these findings in vivo, brains from a transgenic mice deficient for CD45 demonstrate markedly increased production of TNF-α 24 hours after intracerebroventricular injection of Tat (500 ng/mouse) compared to control mice. This increased microglial activation was accompanied by astrogliosis and a significant loss of cortical neurons due to apoptosis in CD45 deficient animals. These results suggest therapeutic agents that activated CD45 PTP signaling may be effective in suppressing microglial activation associated with not only AD, but HAND as well.

Microglia in the Pathogenic Mechanisms Underlying Autism
Carlos A. Pardo-Villamizar, PhD, Johns Hopkins University School of Medicine

Autism spectrum disorders (ASD) are part of neurodevelopmental abnormalities that have produced an important impact on the magnitude of neurological and developmental problems that affect the overall health of the pediatric population. Approximately 1 in 150 children in the United States is diagnosed with any of the autism spectrum disorders. Most of the neurobiological studies demonstrate that the main core of neuropathological abnormalities in ASD are characterized by disturbances in neuronal organization, such as an excessive number of neurons, simplification of dendritic organization and disorganization of cortical lamination. Studies from our laboratory and others have disclosed the role of microglia and neuroimmune responses in cortical regions of brains of children with ASD. These studies support the view that activation of neuroglia cells and neuroimmune mediators such as cytokines, chemokines and signaling pathways such as Toll-like receptors (TLRs) may influence neuronal and synaptic function and contribute to the pathogenic mechanisms and neurobehavioral processes present in ASD. Interestingly, the pattern of neuroglial and innate immune activation follows a pattern of selective involvement of areas of the cerebral cortex known to be dysfunctional in ASD such as the frontal and cingulategyri as well as cerebellum.

An Imbalanced Neuro-immuno-endocrine Set Point as a Cause for Major Mental Disorders
Hemmo A. Drexhage, MD, PhD, Erasmus Medical Center

An imbalanced immuno-endocrine system will be described in patients with severe mental disorders, in individuals at risk for such disorders and in animal models of anxious and schizophrenia-like behavior. This imbalance consists for monocytes/macrophages of over and under expression of coherent sets of activating and suppressing genes (including the glucocorticoid receptor genes) and for the T cell system in raised numbers of both Th1, Th17 and Treg cells. At the level of the microglia such activation does also exist in both patients and animal models (particularly in the hippocampal area), evidence is given that such microglia activation impacts neuronal development and function. Measuring the immuno-endocrine imbalances make predictions for therapy outcome in patients possible.

Seizing Opportunities in Microglial Biology for Epilepsy
Annamaria Vezzani, PhD, Mario Negri Institute for Pharmacological Research

Experimental research has demonstrated a prominent role of glial cells, activated by various brain injuries, in the mechanisms of neuronal damage, seizure precipitation and recurrence, as well as in some neurological dysfunctions often associated with neurodegenerative disorders and epilepsy. In particular, alterations in the phenotype and function of activated astrocytes and microglial cells have been described in experimental and human epileptic tissue, including induction of molecules involved in inflammatory processes. Brain injury can activate innate immune mechanisms involving microglia and astrocytes which in turn release a number of danger signals and proinflammatory mediators, thus initiating a cascade of inflammatory processes in brain tissue. Proinflammatory molecules can alter neuronal excitability and affect the physiological functions of glia by paracrine or autocrine actions, thus perturbing the glio-neuronal communications. In this context, understanding which are the soluble mediators and the molecular mechanisms crucially involved in glio-neuronal interactions is instrumental to shed light on how brain inflammation may contribute to neuronal hyperexcitability, cell loss and maladaptive plasticity in CNS disorders, thus highlighting possible novel therapeutic options.

Microglia, What a (Neuropathic) Pain!
Ru-Rong Ji, PhD, Harvard University and Brigham & Women's Hospital

Neuropathic pain after nerve injury is a growing heath problem. Increasing evidence suggests that peripheral nerve injury induces dramatic changes in spinal cord microglia, such as increased expression of microglia makers (eg., CD11b and Iba1), morphological changes of microglia (hypertrophy), and proliferation of microglia. In particular, nerve injury such as spinal nerve ligation induces dramatic activation (phosphorylation) of p38 MAP kinase selectively in spinal cord microglia. Further, spinal (intrathecal) injection of p38 inhibitor was shown to attenuate nerve injury-induced neuropathic pain symptom in rats and mice, such as mechanical allodynia, pain elicited by normally innocuous mechanical stimulus. Activation of p38 in microglial cells has been shown to induce the expression and release of the proinflammatory cytokines TNF-α and IL-1β and the neurotrophin BDNF. Spinal inhibition of TNF-α, IL-1β, or BDNF has been shown to reduce nerve injury-induced mechanical allodynia. Importantly, microglial mediators can powerfully modulate synaptic transmission in the spinal cord. Specifically, TNF-α, IL-1β, and BDNF can not only increase excitatory synaptic transmission but also decrease inhibitory synaptic transmission in the spinal cord. Thus, activation of spinal cord microglia contributes to the pathogenesis of neuropathic pain via neuron–glial interactions. Targeting microglia signaling may lead to new therapies for the management of devastating neuropathic pain. Finally, I will also discuss new strategies that can inhibit microglia and cytokine signaling for effective pain management.

* Additional abstracts coming soon.

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