Simone di Giovanni, PhD | Imperial College London

Per què els humans fem exposicions? Per què ens agrada o no ens agrada una obra d’art? Quan la mirem, veiem tots el mateix? Per què ens fem preguntes?

Els humans ens fem preguntes des de fa 1,5 milions d’anys, quan vam començar a cuinar. Veurem com aquest fet va fer evolucionar els nostres cervells de manera diferent als altres primats, i això ens ha dut a fascinar-nos pel nostre entorn i ens ha portat a qüestionar-nos i a representar artísticament allò que ens envolta o allò que imaginem. Parlarem de la connexió entre la recerca artística i la recerca científica i parlarem del paper de les neurones en aquesta connexió. També parlarem d’alguns personatges que han estat importants per arribar a saber allò que avui en dia sabem sobre els cervells i veurem que queda molt per descobrir. El futur serà millor si entenem millor el cervell? Volem saber-ne més per poder ajudar en casos de discapacitat mental, de malalties degeneratives o en paràlisis degudes a accidents, i també en casos de transtorns mentals com ara depressions, esquizofrènies, trastorns bipolars... que poden ser malalties molt greus que poden acabar amb la pròpia vida degut a un suïcidi, però ens plantegen molts dubtes sobre la percepció de la realitat i sobre la creativitat... Van Gogh, per exemple, hauria creat el mateix si no hagués patit profundes depressions?

Farem un recorregut per l’exposició mirant l’art a través de les neurones.

Activitat gratuita

Dia Internacional de la dona i la nena en la ciència 2019

Participants:

Mercè Pallas. Catedràtica Universitat de Barcelona. Investigadora principal del grup de Recerca: Medicinal Chemistry and Pharmacology of Neurodegenerative Diseases.

Silvia Ginés. Professora agregada Universitat de Barcelona. Investigadora principal del grup de Recerca: Neurodegeneration and Synaptic Dysfunction in Huntington’s Disease.

Albert Giralt. Investigador Ramón y Cajal del grup de Recerca: Fisiopatologia i Tractament de les Malalties Neurodegeneratives.

Ruth de Diego. Investigadora ICREA Universitat de Barcelona. Investigadora principal del grup de Recerca: Brain Mechanisms of Language Learning.

Marc Via. Professor agregat Universitat de Barcelona. Grup de Recerca: Brain Lab.

Esdeveniment gratuït.

Descripció:

Les trobades a tot el món per al Dia Internacional de les Dones i les Nenes a la Ciència són ocasions per a la celebració, però, més important, són oportunitats per discutir el progrés de les dones joves en aquest camp per convertir-se en líders.

Una àrea de la ciència ha vist específicament el progrés general a nivell nacional i va reunir una atenció global creixent: la neurociència. Les dones han fet contribucions vitals a un ritme accelerat durant les últimes tres dècades a l'hora d'entendre el comportament, l'emoció, el pensament i el funcionament humans. I sembla que la cultura organitzativa i l'impuls personal en aquest camp són les claus de l'èxit.

"La creixent representació de les dones investigadores en neurociències és una tendència prometedora, però encara hi ha més que es pot fer per promoure la seva retenció en l'entorn de la recerca i el progrés en posicions de lideratge en universitats, centres de recerca i el sector privat".

"Continuar investigant per mitigar els biaixos implícits i crear una cultura organitzativa que s'ocupi de l'equilibri entre el treball i la vida són crucials per avançar a les dones en totes les disciplines científiques"

"Seria un retrocés tal si les dones en neurociència es veurien obligades a abandonar la investigació a causa d'un entorn de treball poc acollidor o la manca d'oportunitats clares per a la promoció professional" Dr. Beninson, Board of Higher Education and Workforce at the National Academies of Sciences, Engineering, and Medicine.

“La paraula flexibilitat com a mitjà de com pensem en la recerca, l'avanç científic i la paritat de gènere. Encara que s'han realitzat avanços significatius i s'han aconseguit els èxits, no som on volem ser” Dr. Chiaravalloti, director of Neuropsychology and Neuroscience Laboratory and TBI Research at Kessler Foundation, professor in the Department of Physical Medicine and Rehabilitation at Rutgers - New Jersey Medical School

Dr. Jordi Soriano | Physics Faculty, Universitat de Barcelona

Abstract

Neuronal cultures are a unique system. Their reduced size and ease preparation have made them excellent platforms to investigate a broad range of phenomena in living neuronal networks. Neuronal cultures have become a true interdisciplinary lab-on-a-chip system, fascinating the physical and medical community alike: where the physicists see a grand complex system, the physicians see an extraordinary cross-platform to pinpoint a number of molecular and cellular processes. In this talk I will approach neuronal cultures from the viewpoint of a biophysicist. I will first introduce our main experimental and data analysis tools to investigate the richness of neuronal cultures. Next I will expose the potential –and difficulties– of engineered neuronal cultures to tackle open questions in brain research, including integration-segregation balance and resilience to damage. Along the talk I will introduce different ongoing collaborations that use neuronal cultures as platform to model and arrest neurological disorders.

Jaap Denissen, PhD | Tilburg University

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Michael Rowe, PhD | Yale Department of Psychiatry

Abstract

Citizenship today is often associated with legal citizenship, and especially with who has it and who doesn’t. Yet citizenship is more than its legal status, essential as that status is. Citizenship involves not only our rights and responsibilities in relation to our government, but our relationships with others, our access to resources, and our status as members of our communities and society. In his lecture, Dr. Michael Rowe will: 1) Address the origins of ‘citizenship and mental health’ in the practice of mental health outreach to people who are homeless in the United States; 2)  Review the definition and principles of citizenship in mental health practice; 3) Describe key practices, research, and findings on ‘citizenship work’ in mental health; and 4) Argue for the relevance of citizenship in relation to mental health and community living for people with mental health challenges in other countries, such as Spain.

Sergi Simó, PhD |  University California Davis

Abstract

lopment, neurons migrate, mature, and integrate into the existing network following an intricate set of cues. Similarly, in the adult brain, homeostasis is achieved by responding to cues that regulate a myriad of processes, including adult neurogenesis. Cells respond to all these cues by triggering signaling pathways that, once the information is transduced, must be downregulated. Inappropriate regulation of signaling pathways cause neurons to mismigrate, lose responsiveness to new signals, and/or sustain the original signaling response, causing harm or death to the cell. The E3 Cullin-5 RING ligase (CRL5) is a crucial regulator of neuron migration and cell position in the retina, cortex, and cerebellum, by downregulating the Reelin/Dab1 signaling pathway. However, the role of CRL5 in the developing and adult hippocampus has remained elusive. Our work shows that CRL5 regulates lamination of hippocampal pyramidal neurons and dentate gyrus, mossy fiber innervation, and adult neurogenesis. We demonstrate that CRL5 participates in these events by regulating on at least two different signaling pathways. CRL5 downregulates the Semaphorin-3F signaling pathway to promote mossy fiber axon pruning, establishing proper mossy fiber innervation and opposes the Reelin/Dab1 signaling to control proper adult neurogenesis. Overall, we identified CRL5 as a novel regulator of hippocampal morphogenesis and homeostasis and propose CRL5-regulated signaling pathways involved in these events.

Mark A. Hoon, PhD | National Institutes of Health (NIH), USA

Abstract
The Hoon lab is part of the intramural program of the National Institutes of Health in Bethesda, Maryland, USA. The lab has a general interest in determining the molecular and cellular basis for somatosensory stimulation. They have employed molecular and molecular neuroscience genetic techniques to functionally dissect signaling pathways and defined neurons involved in nociception, thermosensation and itch. The seminar will present work from the lab over the last few years on the delineation of key signaling components and cell involved in itch in mice and potential translatable approaches to alleviate chronic itch.

Abstract submission: open May 13rd / deadline June 14th

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Early Bird Registration: May 13rd / August 31st

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Miriam González Gómez, PhD

Universidad de La Laguna

Abstract

Las neuronas de Cajal-Retzius (NCR) son la principal fuente de reelina en la zona marginal de la neocorteza y el hipocampo (HC) durante el desarrollo prenatal, aunque su producción es complementada por las interneuronas GABAergicas-reelina+ de aparición más tardía. La proteína p73 es imprescindible para la formación de las NCR, dado que están completamente ausentes en el ratón KO-p73. El HC dorsal humano se empieza a formar en la semana gestacional (SG) 10, con el desarrollo de una rudimentaria placa Amónica y una incipiente migración del dentado, aunque la fisura del hipocampo (FH) dorsal se mantiene superficial y contiene pocas NCR. El HC dorsal se transforma en el indusium griseum (IG) con la aparición del cuerpo calloso alrededor de las SG14-17. Los HCs dorsal y ventral se unen en el sitio del antiguo hem caudal, localizado a nivel del futuro atrium del ventrículo lateral e íntimamente conectado con los plexos coroideos. El HC ventral se empieza a formar en la SG11 en el lóbulo temporal. La FH ventral es muy ancha y poco profunda en las SG14-16 y densamente poblada por NCR, éstas están en íntimo contacto con las meninges y los vasos sanguíneos meníngeos, sugiriendo posibles vías de comunicación entre estos componentes. En la SG17, se produce una profundización notable de la fisura y comienza a fusionarse, aunque todavía contiene NCR reelina/p73+. El ratón KO-p73 confirma la importancia de p73 en las NCR para la formación de la FH. En este ratón, las NCR Tbr1/reelina+ nacen en el hem pero no migran y posteriormente desaparecen, por lo que la corteza y el HC del ratón KO-p73 carecen de NCR desde el comienzo de la corticogénesis. La FH está ausente, dando lugar a profundas alteraciones arquitectónicas del HC. Para determinar qué isoforma de p73 es importante para la formación de la FH, hemos estudiado los ratones KO para las isoformas TA y DeltaN durante el desarrollo embrionario y postnatal. En ambos ratones mutados observamos pocas NCR, pero estos fenotipos fueron mucho más leves que el del ratón KO-p73 global. En el ratón KO-TAp73, no se forma la fisura en el HC dorsal pero sí en el HC ventral. En el ratón KO-DeltaNp73, la FH es más corta y el patrón del HC está ligeramente defectuoso. Las complejas interacciones entre ambas isoformas en las NCR pueden contribuir a su actividad crucial en el desarrollo del cerebro.

Late Bird Registration: September 1st / November 13rd

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Louis Bherer, Professor at the Department of Medicine at University of Montréal

Abstract

Physical activity and exercise can help improve cognition, quality of life and mobility in older adults. This talk will be an overview of more than ten years of intervention studies from our lab supporting the notion that multiple exercise modality, from aerobic endurance training to resistance, gross motor exercise and dance training can lead to several benefits in older adults. Our results suggest that these programs can help enhance cognition, quality of life and boost biomarkers associated with brain plasticity (e.g., BDNF).  Studies with patients also suggest that physical activity and exercise can be used as effective non-pharmaceutical intervention in frail older adults and patients with Parkinson’s disease, mild cognitive impairment at dementia.

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Abstract submissions open Thursday, April 11, and close Thursday, May 2.

Abstract submission: open May 13rd / deadline June 14th

Early Bird Registration: May 13rd / August 31st

Late Bird Registration: September 1st / November 13rd

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Josep F. Cheer, Ph.D - University of Maryland School of Medicine

Abstract

It has been posited that compromised motivation in HD or “apathy” arises from a deficit in preparing for and initiating goal-directed behavior. Apathy is always the primary deficit in motivation associated with frontal-subcortical diseases such as HD. Indeed, apathy may be a core feature of HD pathology itself. In many cases apathy follows a similar trajectory as motor symptom progression in HD, although it can become prevalent before phenoconversion. It can be the result of several neurobiologically maladaptive systems, including affective (flattening of emotional responsiveness), behavioral (reduced initiation of spontaneous behavior), and executive dysfunction (difficulty planning/executing). Thus, motivational dysfunction in HD is a deficit primarily in preparation for motivated behavior that can have debilitating co-morbid consequences.

Gaps in knowledge

·      Loss of striatal cannabinoid type 1 (CB1) receptors is a key pathogenic of several neurodegenerative diseases, including HD.

·      Treatment for metabolic syndrome with the CB1 receptor antagonist Rimonabant was halted by the FDA because of loss of motivation and depressive ideation.

·      HD patients tend to smoke marijuana as a way to self-medicate and to prevent feelings of loneliness and helplessness.

·      Loss of goal-directed behavior in HD is specific to the incentive value of the reinforcer.

Treatment with indirect cannabinoid agonists profoundly increases operationally defined indices of motivation in normal animals and reverses apathy via dopaminergic mechanisms in mouse models of HD.

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