Sleep and Cognition

08 July 2017 - 15 July 2017 Certosa di Pontignano, Siena, Italy Open related link

Coordinator: Chiara Cirelli
University of Wisconsin-Madison, Madison. USA


Faculty:

Ian Born, University of Tübingen, Germany

Gyorgy Buzsaki, New York University, USA

Chiara Cirelli, University of Wisconsin-Madison, USA

Derk-Jan Dijk, University of Surrey, UK

Bradley Postle, University of Wisconsin-Madison, USA

Cliff Saper, Harvard University, Cambridge, USA

Giulio Tononi, University of Wisconsin-Madison, USA

The Advanced Course will cut across multiple fields of sleep studies and will feature dedicated sessions addressing important emerging areas. Emphasis will be placed on cutting-edge methods and hypotheses for understanding sleep and its effects on cognitive functions, and on how neurophysiological/genetic/imaging approaches can shed light on the functions of sleep and its essential role in maintaining and preserving vigilance, performance, learning and memory. as well as forgetting. The Advanced Course will be an interactive, multidisciplinary forum in which participants will discard outdated notions, gain an appreciation for the latest thinking, and develop insights that will help navigate the complexity of sleep research.

Neuroepigenetics and Epitranscriptomics

19 August 2017 - 26 August 2017 Certosa di Pontignano, Siena, Italy Open related link

Coordinator: Schahram Akbarian
Icahn School of Medicine at Mount Sinai, New York, USA



Faculty:

Tracy Bale, University of Pennsylvania, Philadelphia, USA

Farah Lubin, University of Alabama School of Medicine, Birmingham, USA

Angel Barco, Instituto de Neurociencias de Alicante, Spain

Art Petronis, Centre for Addiction and Mental Health, University of Toronto, Canada

Ian Maze, Icahn School of Medicine at Mount Sinai, New York, USA

Marcelo Wood, University of California at Irvine, USA


There is increasing evidence that, in addition to DNA sequence and the environment, epigenetic modifications of DNA and histone proteins may contribute to complex phenotypes. Inherited and/or acquired epigenetic factors are partially stable and have regulatory roles in numerous genetic and
genomic activities, thus making epigenetics a promising research path in etiological studies of neuropsychiatric disorders. Methodological and
technological aspects of epigenomic strategies in complex conditions and diseases will be focus of this Advanced Course, looking to understand how
environmental influences or experience-stimuli trigger long-lasting changes in gene transcription and protein synthesis in the brain reflecting in longterm effects. These will provide novel concepts for understanding transcriptional mechanisms subserving neuroadaptation, adult cognition and mental health.

Synaptic and Structural Plasticity

26 August 2017 - 02 September 2017 Certosa di Pontignano, Siena, Italy Open related link

Different forms of synaptic plasticity occurring at the molecular, cellular and circuit level are the focus of this Advanced Course. The Course will start with critical analysis of the evolution of the study of various forms of long-term potentiation and long-term depression and what is generally accepted about their basic mechanisms, including a discussion of modern approaches to understanding the mechanisms and functions of synaptic plasticity. A wide range of areas will be covered, including: (a) the molecular mechanisms underlying different forms of short-term synaptic facilitation and depression that last no more than a few minutes and are typically mediated by presynaptic mechanisms that alter neurotransmitter release (b) the function of key postsynaptic proteins found in the postsynaptic density as well as the role of neurotransmitter receptor regulation during long-term synaptic and experience-dependent plasticity (c) the methodological approaches that have been recently developed to measure the dynamic localization of synaptic elements at nanoscale resolution and how these nanoscale morphological and functional properties regulate synapses (d) the role of neurogenesis throughout life as a crucial mechanism underlying learning-induced circuits in the dentate gyrus and the olfactory bulb (e) how these forms of plasticity integrate to result in the restructuring of entire neuronal circuits.

Participation in the Advanced Course will provide an essential conceptual and methodological framework for anyone intending to pursue rigorous research. The advantages and disadvantages of each method, preparation and recording technique are considered in relation to the specific scientific questions being asked. The Advanced Course will not only develop participants’ skill but will also provide plenty of time for informal gatherings with some of the world leaders in synaptic plasticity, designed to foster brainstorming across different disciplines.

Cognitive Decline and Aging

01 September 2017 - 08 September 2017 Certosa di Pontognano, Siena, Italy Open related link

Coordinator: John H. Morrison
University of California, Davis. USA



Faculty:

Roberta Brinton, University of Southern California, Los Angeles, USA

Mark Baxter, Icahn School of Medicine at Mount Sinai, New York, USA

Tara Spires-Jones, University of Edinburgh, UK

Jennifer Bizon, University of Florida, Gainesville, USA

Naftali Raz, Wayne State University, Detroit, USA

Ulman Lindenberger, Max Planck Institute for Human Development, Berlin, Germany


The interface between cognitive aging that might be considered normal, or at least not devastating, and the early stages of AD has fascinated neuroscientists, neurologists, and perhaps writers for a long time. That interface and whether one is likely to progress from cognitive decline to AD also fills elderly people with fear. This Advanced Course will focus primarily on the events that lead to cognitive decline in the absence of AD, but we will also discuss mechanisms that might be relevant to both conditions. While it is quite clear that the dementia of AD results from neuron death, particularly in circuits that mediate learning and memory, it is equally clear that age-related cognitive decline does not result from neuron death and is thus not a mild form of AD. Age-related cognitive decline appears to result primarily from synaptic alterations and other changes that affect neuronal communication in circuits mediating learning and memory that are still intact. These circuits must retain synaptic health in order to function properly, and certain events associated with aging lead to declining synaptic health. What is the nature of these age-related alterations and what causes them? Can they be prevented or treated? What are the mechanisms involved in synaptic aging and are they in any way similar to those implicated in neuron death? How do these synaptic alterations lead to cognitive decline? Why is cognition so vulnerable to aging? Do brain regions age differently and at different rates? Are there changes across the lifespan or does cognitive aging and its neurobiological causes occur suddenly? We will address these issues and more in this Advanced Course.

Single Cell Omics

17 September 2017 - 24 September 2017 Certosa di Pontignano, Siena, Italy Open related link

Coordinator: James Eberwine
University of Pennsylvania, USA


Co-Coordinator: Scott Fraser
University of Southern California, Los Angeles, USA



Faculty:

James Eberwine, University of Pennsylvania. USA

Scott Fraser, University of Southern California, Los Angeles. USA

Thierry Voet, KU Leuven, Belgium

Sarah Teichmann, Sanger Institute, Hinxton, UK

Jin Zhang, University of California, San Diego, USA

Amy Herr, University of Berkeley, USA

Jonathan Sweedler, University of Illinois, Chicago, USA

Neuroscience has entered a critical phase, with several international large-scale efforts devoted to the analysis and understanding of brain function. Studies exploiting new technologies for defining the connections in the brain, driving neuronal activity and modeling of neuronal processing are each hampered by our incomplete knowledge of the brain’s constituent parts. Fortunately, a bevy of single cell analyses are now being deployed to better understand the cells that constitute the functioning nervous system. These approaches offer insights into how cells function individually as the building blocks for understanding how they work in ensemble to create functional pathways.

A set of emerging tools are available to assess the molecular and cell biology of single cells, including genomic analyses of somatic mutations, epigenomics to explain the influence of the environment upon genome expression, and transcriptomics to gain insight into the capacity of a cell to synthesize proteins and modulate its environment. Powerful technologies permit a variety of cell constituents to be addressed, including proteins, post-translational modifications, peptides and metabolites. Novel biosensors offer parallel analyses of cellular physiological states, reporting on the pH, membrane voltage and metabolic state. Multiplexed together, such methodologies offer a far more complete biological understanding than the more typical gene expression analyses, providing a rich picture of each single cell’s biology in their normal context – information needed to fully interpret the meaning of results from transcriptomics and proteomics studies. This Advanced Course is designed to provide the foundational knowledge needed to critically evaluate the design and execution of single cell omic studies, through daily lectures by the Faculty, critical reading of papers and extensive didactic discussion sessions. In the sessions, discussion will focus on the proper framing of scientific questions to best utilize these techniques, the limitations and advantages of each technique, and what the data can tell us about neuronal function.

The Neuroscience of Obesity

17 September 2017 - 24 September 2017 Certosa di Pontignano, Siena, Italy Open related link

Coordinator: Tamas Horvath
Yale University, New Haven. USA


Scott Sternson, HHMI, Janelia Research Farms, Ashburn, USA

Sabrina Diano, Yale University, New Haven, USA

Matthias Tschöp, Helmholtz Zentrum and Technical University, Munich, Germany

Jens Bruning, Max Planck Institute for Metabolism Research, Cologne, Germany

Tibor Harkany, Karolinska Institute, Stockholm, Sweden

Giovanni Marsicano, Neurocentre Magendie, Bordeaux, France

Significant progress has been made in recent years in the understanding the role of the nervous system in obesity. Not only several different neuronal pathways, neurotransmitters and hormones have been identified as major players in the regulation of feeding and body weight, bu also energy balance in mammals is controlled by a complex network of interacting feedback mechanisms that involve peripheral organs in addition to higher brain centers.

This Advanced Course will provide conceptual- and cutting edge technological framework for state-of-the-art of neuroscience on energy metabolism. The Faculty represents diverse expertise in molecular, cellular, circuit and behavioral approaches on contemporary questions regarding the role of the brain in systemic metabolism regulation and how the periphery affects complex brain functions via neuronal circuits and brain cells.