See also the schedule on the Events Calendar page
DATE AND TIME: Postponed date to be confirmed, 2016 – h. tbcLOCATION: tbc Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public
SPEAKER: Maria Eriksdotter – Professor of Geriatrics at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet
TITLE: tbcABSTRACT :
SPEAKER: Prof. Dr. Mark Hübener, Max Planck Institute of Neurobiology, Martinsried, Germany
TITLE: “Plasticity of old and new neurons in the visual cortex”ABSTRACT :In this lecture, I will present recent data from our group, that the one hand address behaviorally relevant plasticity among mature neuron in the adult cortex, and on the other hand describe how new neurons transplanted into the adult visual cortex integrate into existing neuronal circuits.To study the neuronal basis of associative visual memory formation, we use several approaches, among them complex types of visual based learning, such as category learning. To this end, we defined two categories of grating stimuli by introducing a category boundary in a two-dimensional stimulus space consisting of gratings that varied continuously in orientation and spatial frequency. Mice learned to discriminate these two categories in a head- restrained two-choice paradigm. We are using chronic two-photon calcium imaging in higher visual areas of the visual cortex to identify neurons representing learned categories, ultimately allowing us to study the synaptic changes underlying category learning.In order to study whether new neurons can integrate into existing circuits, we chronically image the fate of embryonic neurons transplanted into the visual cortex of adult mice. Such transplanted cells mature into bona-fide pyramidal cells with selective pruning of basal dendrites, achieving adult-like densities of dendritic spines and axonal boutons within 4-8 weeks. Monosynaptic tracing reveals that grafted neurons receive area-specific, afferent inputs matching those of pyramidal neurons in the normal visual cortex. Furthermore, selective responses to visual stimuli refine over the course of many weeks and finally become indistinguishable from those of host neurons. Thus, grafted neurons can integrate with great specificity into neocortical circuits that normally never incorporate new neurons in the adult brain.
DATE AND TIME: Wednesday, November 4, 2015 – h. 12.00 LOCATION: Aula Bianchi Scienze Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Mohamed H. Farah, PhD, Assistant Professor – Department of Neurology Johns Hopkins School of Medicine
TITLE: “Augmenting axon plasticity in motor neuron disease and diabetic neuropathy models”ABSTRACT : Dr Farah’s lab works on research project that involves intersection of nerve-immune cells in axonal regeneration, basic cellular and molecular investigations into nerve regeneration, and preclinical testing of compounds that might accelerate nerve regeneration in motor neuron disease and diabetic peripheral neuropathy mouse models POSTER_MohamedFarah
DATE AND TIME: Wednesday, November 18, 2015 – h. 12.00 LOCATION: Aula Bianchi Scienze Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Andrea Nistri Full professor of Cellular and Molecular Pharmacology at SISSA, Scuola Internazionale Superiore di Studi Avanzati
TITLE: “Basic mechanisms of migraine pain”ABSTRACT : Migraine is a common and disabling neurological disease worldwide. While the origin of the headache remains controversial, it is clear that activation of nociceptive sensory neurons in trigeminal ganglia is a major process to generate pain. These neurons constitutively express membrane proteins, termed P2X3 receptors that transduce a chemical signal into nociception. Is it possible to up or downregulate P2X3 receptor function to prevent or trigger headache? Certain answers to these questions are obtained by studying migraine mouse models expressing a common mutation of human hereditary migraine. A talk on “Authorship” of Scientific Publications will be given by Prof. Nistri on the same afternoon
DATE AND TIME: Wednesday, December 2, 2015 – h. 12.00 LOCATION: Aula Russo Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Laura Cancedda, Dept. of Neuroscience and Brain Technologies, Italian Institute of Technology (IIT)
TITLE: Cellular Environment: Implication for Brain Development and Maldevelopment
ABSTRACT: What are the fundamental cellular mechanisms that control the development of the cerebrum and how these events relate to the fine cortical wiring and ability of the brain to respond to environmental stimuli? Common knowledge indicates two distinct yet intermingled phases fundamental for brain development. The first phase is mainly regulated by genetic programs and spontaneous activity, whereas the second phase is characterized by a strong influence of the external environment conveyed to the brain through sensory systems. Recent work in the lab. has focused on the novel conceptual framework of “cellular environment”, which can be considered as a third phase of brain development that would stand in between the gene-driven and sense-driven phases. This concept entails the idea that the extracellular milieu of a specific developing brain cell is characterized by the presence of other cells that are developing themselves and possibly influence each others. However, as development is by definition a dynamic process, cellular environment will constantly change over time and it will be different in different brain areas. This implies that what may be relevant for a specific developmental process at a given time in a particular brain area may not be significant at another time or place due to different cellular environments. Finally, this has tremendous conceptual consequences for the treatment of neurodevelopmental disorders, as the study of the different cellular environments during brain development may eventually lead to individuating specific therapeutic windows to address aberrant neuronal development with much reduced side effects. I will present recent data from the lab describing technical developments for the study of cellular environment and experimental evidence indicating a role for aberrant cellular environment in the brain development of a mutant mouse characterized by autism-like behaviors.
DATE AND TIME: Thursday, December 10, 2015 – h. 12.00 LOCATION: Aula Bianchi Scienze Pallazzo della Carovana Scuola Normale Superiore Piazza dei Cavalieri, 7 Pisa ATTENDEES: Open to the public SPEAKER: Helen Morrison, Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) Helen Morrison, Ph.D. is a group leader at the Leibniz-Institute of Age Research – Fritz Lipmann Institute (FLI) in Jena, Germany. She has served on several national and international review panels and has authored numerous peer-reviewed manuscripts. Her interest is the nature of cell communication, and the mis-wiring of signalling pathways in disease and in the ageing process. Specifically, her focus is on age dependent signalling impairments underlying nervous system maintenance and regeneration, and in disease mechanisms for disorders of myelinating cells and brain tumours. Dr. Morrison has extensive experience in NF2 research including dissecting NF2 signalling pathways.
TITLE: Healing and Tumour formation
ABSTRACT: Schwannomas are benign nerve sheath neoplasms caused by NF2 gene inactivation. Presently, treatment options are mainly limited to surgical tumor resection. Although the mechanistic understanding ofNF2 gene function has advanced, it is primarily restricted to Schwann cell-intrinsic events. Conversely, extracellular cues determining Schwann cell behaviour with regard to schwannoma development remain profoundly obscure. Here we investigate pro-tumourigenic axonal effects on Schwann cells in genetically engineered mice where nerve repair processes promote schwannoma development. Specifically, we found patient-mimicking schwannomas could be induced by crush injury in animals with combined heterozygous nf2 deletion in Schwann cells and axons. We identified a severe re-myelination defect in combination with sustained macrophage infiltration as underlying cause. Taken together, our results suggest a multifactorial concept for schwannoma formation emphasizing microenvironmental factors, incomplete nerve regeneration after injury and dispensability of loss of heterozygosity.
DATE AND TIME: Wednesday, December 16, 2015 – h. 12.00 LOCATION: Aula Russo Scuola Normale Superiore Pallazzo della Carovana Piazza dei Cavalieri, 7 Pisa ATTENDEES: Open to the public SPEAKER: Maria Concetta Morrone, Department of Translational Research on New Technologies in Medicine and Surgery, University of Pisa – Fondazione Stella Maris IRCCS
TITLE: Development and plasticity of primary visual cortex in humans
ABSTRACT: The brain is flexible, and continuously adapts to past experience, moulding cortical circuitry to optimally analyse incoming information. In this talk, I will give two examples of visual cortical plasticity, one in adult life and one during development. We have recently demonstrated that plastic changes in primary visual cortex are not limited to the developmental period, but can extend through life. We showed strong residual plasticity particularly for processes involving competition between ocular inputs. One of the most sensitive measures of the effects of deprivation is binocular rivalry, a form of visual bistability that engages strong competition between monocular signals. Surprisingly, short-term monocular deprivation results in the deprived eye dominating rivalrous perception, lasting up to 3h after patch removal. Our results suggest that monocular deprivation may act to up-regulate contrast gain, resulting in stronger signals from the deprived eye (homeostatic plasticity, contrary to what is thought to occur with patching therapy). We further show a release of GABAergic inhibition after short deprivation in occipital cortex measured by MR spectroscopy at 7T. In summary, the adult human visual cortex retains a high degree of plasticity using similar molecular mechanisms at core function in modulating plasticity during development. To understand cortical plasticity in humans, we need to understand better how the cortical circuits develop during early post-natal age. Vision in young infants is very limited. However, using fMRI, we have demonstrated unexpected maturation of the cortical circuitry that is selective to motion direction in young infants. BOLD responses to flow-motion versus random-motion in 7-week-old infants are nearly adult-like in parietal-occipital area, cuneous, posterior parietal and posterior insular cortex, which in adults receives visual-vestibular input. We also have evidence that MT receives independent input from V1 perinatally, and that V1 maturation is delayed with respect to other cortical visual area. This may help to explain the profound reorganization that we and others have observed in patients with perinatal lesions of optical radiation, where ipsilateral primary cortex codes non only the contralateral but also the ipsilateral visual field.
DATE AND TIME: Wednesday, January 27, 2016 – h. 12.00LOCATION: Aula Russo Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Vincenzo Lionetti,TRANCRILAB, Sector of Medicine, Institute of Life Sciences, Scuola Superiore Sant’Anna, Pisa
TITLE: The dark side of the heart is the brain
ABSTRACT: The formation of the heart is controlled by intrinsic and extrinsic signals, and crosstalk between different type of cells. Cardiac neural crest cells migrate from the dorsal neural tube to participate in cardiogenesis. However, the tracks of these cells are lost suddenly during the progression of development and functional maturation of the heart. Even though many neurons and nerve fibers reside between adult cardiomyocytes, it is not yet clear the role played by cells originating from the neural crest in the function of the adult heart. Recent evidences have shown that cardiomyocytes of a failing human heart express neural proteins, such as nestin.Nestin is a type VI intermediate filament protein expressed mostly in neurons, where they are implicated in the radial growth of the axon, and also in neural stem cells. To date it is not known the source of nestin-positive cardiomyocytes and the role played by nestin in adult heart. Some investigators suggest that nestin-positive cardiomyocytes derive from neural stem cells. Conversely, we have demonstrated that increased nestin expression in adult cardiomyocytes prevents apoptosis without de-differerentiating the cells, and recapituales the benefits of fetal reprogramming of cardiomyocytes under stress.Our findings reveal a hitherto unsuspected profile of stressed adult cardiomyocytes and open new avenues in cardiac protection/repair.
DATE AND TIME: Thursday, February 18, 2016 – h. 11.00LOCATION: Aula Dini Palazzo del Castelletto Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Giovanna Mallucci, Department of Clinical Neurosciences, University of Cambridge (http://tox.mrc.ac.uk/research/mallucci-group/)
TITLE: “neurodegeneration: from mechanisms to medicines”
ABSTRACT:This talk will cover our recent progress in understanding mechanisms of neurodegeneration and how this is informing new therapeutic approaches. The central concept is the identification of common pathways across the spectrum of these disorders (which include Alzheimer’s and related diseases) that are relevant for both mechanistic insights and therapy. These include both ‘toxic’ processes that can be targeted to prevent neuronal death, and regenerative processes that can be harnessed for repair. I will discuss our data in mouse models targeting both of these aspects to prevent neurodegeneration and their relevance for human disease.
DATE AND TIME: Wednesday, February 24, 2016 – h. 12.00LOCATION: Sala Stemmi Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Michela Matteoli, Director of Neurological Research Area and Head of Lab, Pharmacology and Brain Pathology Lab, Humanitas Clinical and Research Center and Institute of Neuroscience CNR (http://www.humanitas-research.org/category/principal-investigator/matteoli/)
TITLE: “How the immune system affects synaptic function”
JOINT SEMINAR Seminari Frontiere della Chimica/seminari di NeuroscienzeDATE AND TIME: Wednesday, March 2, 2016 – h. 14.00 LOCATION: Aula Mancini Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Ranieri Bizzarri(NEST, Istituto Nanoscienze – CNR, piazza San Silvestro 12, 56127 Pisa) TITLE: “New Optical probes and Imaging Strategy for Biology and Biomedicine” DOWNLOAD ABSTRACT (PDF)
DATE AND TIME: Wednesday, March 16 (tbc), 2016 – h. 12.00LOCATION: Sala Azzurra Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Silvestro Micera, The BioRobotics Institute, Scuola Superiore Sant’Anna, Pisa, Italy and Bertarelli Foundation Chair in Translational NeuroEngineering, Center for Neuroprosthetics, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland
TITLE: Neuroprosthetics for a better life: current achievements and future perspectives
ABSTRACT: Neuroengineering is a novel discipline combining engineering including micro and nanotechnology, electrical and mechanical, and computer science with cellular, molecular, cognitive neuroscience with two main goals: (i) increase our basic knowledge of how the nervous system works; (ii) develop systems able to restore functions in people affected by different types of neural disability. In the past years, several breakthroughs have been reached by neuroengineers in particular on the development of neurotechnologies able to restore sensorimotor functions in disabled people.
In this presentation, after a general introduction about the results achieved so far by neuroprosthetic systems, two main research activities on this topic carried out by my laboratory in the past years will be presented. First, the recent results achieved after the implantation of intraneural electrodes in an amputee will be presented. We showed that using this approach it is possible to restore the bidirectional connection between a dexterous hand prosthesis and the nervous system. The user was also able to improve his ability to provide useful motor commands over time.
Then, I will show the results achieved in collaboration with Prof. Courtine at EPFL to restore locomotion using epidural electrical stimulation after spinal cord injury in rats.
Finally, a brief description of neuroprosthetics possible future achievement will be also provided.
DATE AND TIME: Friday, April 1, 2016 – h. 14.30 (tbc)LOCATION: Aula Bianchi Scienze Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Pierre Baldi, University of California in Irvine (UCI), School of Information and Computer Sciences (ICS), Institute for Genomics and Bioinformatics (IGB)
TITLE: Molecular Systems Biology of Circadian Rhythms
ABSTRACT: Circadian rhythms date back to the origins of life, are found in virtually every species and every cell, and play fundamental roles in functions ranging from metabolism to cognition.
These rhythms play also important roles in health and disease states and should be taken into account in precision medicine, for instance to determine the optimal time at which a drug should be taken. Modern high-throughput technologies allow the measurement of concentrations of transcripts, metabolites, and other species along the circadian cycle under a variety of conditions, thus creating novel computational challenges and opportunities for improving our fundamental understanding of circadian biology and its applications to precision medicine. We will present several experimental results that have led to the development of new computational tools in circadian biology, including a general framework for understanding the pervasiveness and plasticity of circadian rhythms at the molecular systems biology level. We will also present deep machine learning methods to detect periodicity in time series and impute time from a set of high-throughput measurements, two necessary prerequisites for the application of circadian biology to precision medicine.
V. Patel, N. Ceglia, M. Zeller, K. Eckel-Mahan, P. Sassone-Corsi, and P. Baldi. The Pervasiveness and Plasticity of Circadian Oscillations: The Coupled Circadian-Oscillators Framework. Bioinformatics 31 (19): 3181-3188, (2015).
K. L. Eckel-Mahan, V. R. Patel, S. de Mateo, N. J. Ceglia, S. Sahar, S. Dilag, K. A. Dyar, R. Orozco-Solis, P. Baldi, and Paolo Sassone-Corsi. Reprogramming of the Circadian Clock by Nutritional Challenge. Cell, 155, 7, 1464-1478, (2013).
V. Patel, K. Eckel Mahan, P. Sassone-Corsi, and P. Baldi. CircadiOmics: Integrating Circadian Genomics, Transcriptomics, Proteomics, and Metabolomics. Nature Methods, 9, 8, 772-773, (2012).
K. L. Eckel-Mahan, V. R. Patel, K. S.Vignola, R. P. Mohney, P. Baldi, and P. Sassone-Corsi. Coordination of Metabolome and Transcriptome by the Circadian Clock. PNAS, 109 (14) 5541-5546; published ahead of print March 19, 2012.
DATE AND TIME: Wednesday, April 27, 2016 – h. 14:30LOCATION: Sala Conferenze Collegio Puteano Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Andrew Johnson, Professor of Cell and Developmental Biology, Faculty of Medicine & Health Sciences
TITLE: The Germ Line is Master of Its Own Destiny
ABSTRACT: The germ line transmits genetic information across generations, and it is the source of genetic diversity. However, given its unique role in evolution, it is surprising that many different molecular mechanisms have evolved to regulate germ line development in metazoans. I will present the hypothesis that these diverse mechanisms evolved in the animal kingdom to enhance species diversity. This model predicts that the mode of germ line development has shaped the pattern of metazoan natural history, and has obscured our understanding of how mechanisms for vertebrate development evolved.
DATE AND TIME: Wednesday, May 11, 2016 – h. 12:00LOCATION:
TITLE: Under the skin: Decoding the molecular basis of touch sensation
ABSTRACT : The sense of touch and pain is fundamentally important for life. However, how force is sensed at the molecular level is largely unknown. At its most fundamental level, touch sensation requires the translation of mechanical energy into mechanosensitive ion channel opening, thereby generating electrochemical signals. Here I describe our work on understanding how the cytoskeleton, in particular microtubules, influences touch sensation. Focusing on conditional knockout mice for the α-tubulin acetyltransferase Atat1, I will show how these mice display profound deficits in their ability to detect mechanical stimuli, and are largely insensitive to mechanical touch and pain. I will explore the mechanistic basis of this phenotype, showing how acetylated tubulin contributes to the stiffness of sensory neurons. This simple physical property reduces the ability of neurons to transduce mechanical stimuli, which in turn has fundamental consequences for how an organism detects its environment.
DATE AND TIME: Wednesday, May 18, 2016 – h. 15:00LOCATION: Sala Conferenze Collegio Puteano Piazza dei Cavalieri 3, Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Antonello Mallamaci, Associate Professor in Molecular Biology and Head of the Laboratory of Cerebral Cortex Development, SISSA Trieste
TITLE: Emx2 inhibits cortico-cerebral astrogenesis and suppresses glioblastoma – RNA therapeutics of neural genes haploinsufficiencies
ABSTRACT : Transcription factor genes governing early patterning of rostral CNS are often still active in patterned proliferating precursors, tuning key parameters of their histogenetic activity. Among such factors there is Emx2. We previously addressed its pivotal role in pallial specification of dorsal telencephalon, areal profiling of the cortical primordium and proper spatio-temporal modulation of cortical neuronogenic rates. Here, we show that Emx2 further contributes to postpone the bulk of astrogenesis to neuronogenesis, by antagonizing proliferation of astrocyte-committed progenitors. Consistently, its over-expression supresses glioblastoma multiforme, a devastating brain tumour for which no cure is presently available.
Remarkably, proper allele dosage is often crucial to fine histogenetic control exerted by neural patterning genes and gene haploinsufficiency underlies an increasing number of rare neurodevelopmental-neurophysiological disorders, for which no therapy is presently available. Specific RNA-based devices offer innovative approches to address this issue. In this respect, here we review our work on artificial miRNA-like activators of transcription as well as on NMHVs, a novel class of programmable, ribonucleoproteic transcription factors we recently created.
DATE AND TIME: Thursday, May 19, 2016 – h. 15:00LOCATION: Sala Conferenze Collegio Puteano Piazza dei Cavalieri 3, Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Joachim Schulz and Antonio Bonucci European XFEL GmbH
TITLE: European XFEL: overview of the project and opportunity for the Biology
ABSTRACT : The Hamburg area will soon boast a new state-of-the-art research facility: The European XFEL will generate ultrashort X-ray flashes—27 000 times per second and with a brilliance that is a billion times higher than that of the best conventional X-ray radiation sources. The outstanding characteristics of the facility are unique worldwide. Starting in 2017, it will open up completely new research opportunities for scientists and industrial users.
Smaller, faster, more intense: The European XFEL will open up areas of research that were previously inaccessible. Using the X-ray flashes of the European XFEL, scientists will be able to map the atomic details of viruses, decipher the molecular composition of cells, take three-dimensional images of the nanoworld, film chemical reactions, and study processes such as those occurring deep inside planets.
To generate the X-ray flashes, bunches of electrons will first be accelerated to high energies and then directed through special arrangements of magnets (undulators). In the process, the particles will emit radiation that is increasingly amplified until an extremely short and intense X-ray flash is finally created.
Depending on the experimental requirements, the X-ray flashes can be widened, focused, filtered, or weakened using optical elements such as mirrors, gratings, slits, or crystals. The samples are provided in the experiment station, where they interact with the X-ray flashes. The results of these interactions are measuredusing special detectors. The data is recorded and processed for analysis. The researchers can follow the progress of the experiments from a neighbouring control room.
In this seminar, the main opportunities of the experimental instruments and the characteristics of the sample environment will be presented.
DATE AND TIME: Wednesday, June 8, 2016 – h. 15:00LOCATION: Sala Azzurra Palazzo della Carovana Piazza dei Cavalieri 7, Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Pier Giuseppe Pelicci, Istituto Europeo di Oncologia (IEO), Milan, Italy and Department of Oncology and Haemato-oncology, University of Milan, Italy
TITLE: Regulation of self-renewal in cancer stem cells
Recent findings support the concept that cells with the properties of stem cells (SC) are integral to the development and perpetuation of several forms of human cancer, and that eradication of cancer stem cells (CSC) may be essential to achieve cancer cure. However, direct proof of these concepts is still lacking, mainly due the scarcity of appropriate model systems. We have recently defined a number of CSC-specific biological properties and underlying molecular mechanisms, using mouse models of i) leukaemia, obtained by transgenic expression of the PML-RAR, mutant NPM or AML1-ETO leukemia-associated oncogenes; and ii) mammary tumor, obtained by transgenic expression of the ErbB2 oncogene. We found that self-renewing divisions of CSCs are more frequent than normal counterparts, unlimited and symmetric, thus contributing to increasing numbers of SCs in tumoral tissues. SCs with targeted mutation of the tumor suppressor p53 possess the same self-renewal properties of cancer SCs, and their number increases progressively in the p53-null pre-malignant mammary gland. We showed that p53 signaling is attenuated in ErbB2-driven tumors, and that pharmacological re-activation of p53 induced restoration of asymmetric divisions in cancer SCs and tumor growth reduction, without affecting rates of apoptosis or proliferation on additional cancer cells. These data demonstrate that p53 regulates polarity of cell division in mammary SCs and suggest that loss-of-p53 in epithelial cancers favors symmetric divisions of CSCs, contributing to tumor growth. As a further mechanisms of extended self-renewal in cancer stem cells, we have demonstrated that up-regulation of the cell-cycle inhibitor p21 is indispensable for maintaining self-renewal of leukaemia SCs (LSCs). Expression of leukaemia-associated oncogenes in normal hematopoietic SCs (HSCs) induces DNA damage and activates a p21-dependent cellular response that, in turn, imposes cell-cycle restriction and triggers repair of the damaged DNA. This effect of p21 prevents the physiological exhaustion of HSC self-renewal, which occurs in time owing to accumulation of DNA damage, and confers an advantage to HSCs when they hyper-proliferate, as it occurs during stress or after full transformation (for example, in the LSCs), thus explaining the role of p21 in the maintenance of the self-renewal potential of LSCs. Finally, I will discuss unpublished data showing the contribution of immune-surveillance to the elimination of DNA-damaged SCs, and the underlying role of p21.
DATE AND TIME: Wednesday, June 15, 2016 – h. 15:00LOCATION: Sala Conferenze Palazzo Puteano Piazza dei Cavalieri, 3 Scuola Normale Superiore Pisa ATTENDEES: Open to the public SPEAKER: Prof. Dr Ivanka Markovic, Institute of Medical and Clinical Biochemistry, Faculty of Medicine, University of Belgrade
TITLE: Adenosine monophosphate-activated protein kinase in Parkinson’s disease – friend or foe?
The exact molecular mechanism leading to pathogenesis of Parkinson’s disease (PD) is still insufficiently elucidated but wide range of studies implicates aberrant mitochondrial homeostasis as a key contributor in PD development. An increasing body of evidence shows that dysfunctional mitochondria and all of the resultant features are related to adenosine monophosphate–activated protein kinase (AMPK) signaling pathway. The AMPK is a sensor of cellular energy status, expressed in essentially all eukaryotic cells, which plays important roles in regulating important cellular processes such as autophagy and mitochondrial biogenesis. Alterations of AMPK signaling have been demonstrated in several brain diseases. In the case of PD, AMPK activation appears to function as a double-edged sword, promoting or aggravating neurodegeneration, which appears to be cell type- and/or context-dependent. This talk will elaborate the role of AMPK metabolic pathway in different PD models (intra- and extracellular alpha-synuclein overexpression, MPP+ neurotoxic model), its effect on mitochondrial function and interplay with other signaling pathways. Special emphasis will be made on possibilities for AMPK activity modulation as neuroprotective strategy in PD.DATE AND TIME: Wednesday, October 19, 2016 – h. 12.00 LOCATION: Sala Stemmi Pallazzo della Carovana Scuola Normale Superiore Pisa ATTENDEES: Open to the public