Miquel Vila Bover Sóc investigador ICREA i dirigeixo el Grup de Recerca en Malalties Neurodegeneratives del Vall d’Hebron Institut de Recerca (VHIR) Institucions de les que formen part Cap de grup Malalties neurodegeneratives Vall Hebron Institut de Recerca Miquel Vila Bover Institucions de les que formen part Cap de grup Malalties neurodegeneratives Vall Hebron Institut de Recerca Sóc investigador ICREA i dirigeixo el Grup de Recerca en Malalties Neurodegeneratives del Vall d’Hebron Institut de Recerca (VHIR)
Sóc llicenciat en Medicina i Cirurgia per la Universitat de Barcelona (1993) i Doctor en Neurociències per la Universitat de Paris 6 (1998). El meu treball de doctorat realitzat al laboratori de neurologia experimental de l’Hospital de la Salpêtrière de Paris (1993-98) va contribuir a establir el nucli subtalàmic com a principal diana terapèutica per al tractament quirúrgic de la malaltia de Parkinson amb estimulació cerebral profunda. De 1998 a 2005 vaig treballar a la Unitat de Transtorns del Moviment de la Universitat de Columbia de Nova York (USA), inicialment com a investigador postdoctoral i des de 2001 com a Professor titular de neurologia d’aquesta universitat, centrat en l’estudi dels mecanismes de mort neuronal en la malaltia de Parkinson per identificar noves dianes terapèutiques per aquesta malaltia. L’any 2006 em vaig traslladar a Barcelona com a Professor d’Investigació ICREA (Institució Catalana de Recerca i Estudis Avançats) per fundar i dirigir un nou grup de recerca en malalties neurodegeneratives al Vall d’Hebron Institut de Recerca (VHIR). Des de llavors, el nostre grup s’ha consolidat com a referent en l’estudi de la malaltia de Parkinson i forma part del Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas (CIBERNED) i de l’Aligning Science Across Parkinson’s Collaborative Research Network (ASAP-CRN). També sóc professor associat a la Universitat Autonòma de Barcelona, investigador principal del CIBERNED, investigador principal coordinador de l'ASAP-CRN i membre dels Comitès de Direcció de la World Parkinson Coalition i del Basic Science Special Interest Group de la International Parkinson and Movement Disorder Society.
Línies de recerca Regeneration of dopaminergic neurons in Parkinson's disease via cell fusion-mediated reprogramming Co-PI: Pia Cosma, CRG. Given the current lack of disease-modifying therapies for Parkinson’s disease (PD), we are exploring whether cell-fusion-mediated regeneration of dopaminergic neurons can be achieved, for therapeutic purposes, in experimental animal models of PD after transplantation of Wnt-activated haematopoietic stem and progenitor cells (HSPCs). IP: Miquel Vila Bover Pathogenic role of autophagic/lysosomal dysfunction in Parkinson's disease Autophagy is the degradation of intracellular components inside the lysosomes and it is essential for the maintenance of cellular homeostasis and neuronal viability. Alterations in the autophagy process have been associated with neurodegenerative diseases including Parkinson’s, Huntington’s and Alzheimer’s disease and has been shown to be one of the main causes that contribute to neuronal death in these pathologies. Our efforts are currently directed to: - Development of new therapies for Parkinson’s disease based in the restoration of lysosomal glucocerebrosidase (GBA) activity. - Development of new autophagy pharmacological modulators (mTOR-independent) as a therapeutic strategy in neurodegenerative diseases. IP: Marta Martínez Vicente, Miquel Vila Bover Role of mitochondria in Parkinson's disease Mitochondria are highly dynamic organelles with complex structural features that play several important cellular functions, such as the production of energy by oxidative phosphorylation, the regulation of calcium homeostasis, or the control of programmed cell death. Given its essential role in neuronal viability, alterations in mitochondrial biology can lead to neuron dysfunction and cell death. Defects in mitochondrial respiration have long been implicated in the etiology and pathogenesis of Parkinson's disease (PD). However, the role of mitochondria in PD extends well beyond defective respiration and also involves perturbations in mitochondrial dynamics, leading to alterations in mitochondrial morphology, intracellular trafficking, or quality control. Whether a primary or secondary event, mitochondrial dysfunction holds promise as a potential therapeutic target to halt the progression of dopaminergic neurodegeneration in PD. IP: Miquel Vila Bover Alpha-synuclein involvement in Parkinson's disease Formation and accumulation of abnormal protein aggregates are a central hallmark of several neurodegenerative diseases. In Parkinson’s disease (PD), the aggregation-prone protein á-synuclein accumulates in several areas of the central and peripheral nervous system. Pathological á-synuclein accumulation in PD can result from (i) abnormally increased á-synuclein expression, (ii) defective intracellular clearance of á-synuclein protein, (iii) progressive self-propagation and spreading of pathological á-synuclein between interconnected brain areas. Targeting á-synuclein pathological changes may provide therapeutic benefit to delay, halt or prevent neuronal dysfunction and degeneration in PD. IP: Miquel Vila Bover Paginació Pàgina actual 1 Page 2 Pàgina següent › Última pàgina » Projectes Malalties neurodegeneratives IP: Miquel Vila Bover Col·laboradors: Jorge Hernández Vara, Joan Compte Barrón, Marta Martínez Vicente, Jordi Bove Badell, Eddie Pradas Gracia, Maria Camprodon Gomez, Núria Peñuelas Peñarroya, Camille Guillard Sirieix, Marina Lorente Picón, Laura Castillo Ribelles, Oriol de Fabregues-Boixar Nebot, Javier Hoyo Pérez, Ariadna Laguna Tuset, Thais Cuadros Arasa, Jordi Riera Heredia, David Ramos Vicente, Marta Montpeyó Garcia-Moreno, Maria Sellés Altés, Helena Xicoy Cortada, Alba Nicolau Vera, Marta González Sepúlveda, Anna Garcia Serra, Joana Margalida Cladera Sastre, Annabelle Parent , Daniela Samaniego Toro, Daniela Samaniego Toro Entitat finançadora: AGAUR no fer servir-correcte 4301-37 Finançament: 40000 Referència: 2021 SGR 00784 Durada: 01/01/2022 - 31/12/2024 MECANISMOS MOLECULARES DE NEURODEGENERACION LIGADA A LA NEUROMELANINA EN LA ENFERMEDAD DE PARKINSON Y ENVEJECIMIENTO CEREBRAL IP: Miquel Vila Bover Col·laboradors: Gerard Roch Alba, Miriam Izquierdo Sans Entitat finançadora: Ministerio de Ciencia e Innovación-MICINN Finançament: 99260 Referència: PRE2021-098300 Durada: 01/07/2022 - 30/06/2026 Activity and connectivity drive neuronal vulnerability and disease progression in Parkinson's disease IP: Miquel Vila Bover Col·laboradors: Joan Compte Barrón, Javier Hoyo Pérez, Gerard Roch Alba, Marta González Sepúlveda, Ariadna Laguna Tuset, Joana Margalida Cladera Sastre, Núria Peñuelas Peñarroya Entitat finançadora: Michael J. Fox Foundation Finançament: 1269495.05 Referència: ASAP_MJFF2021 Durada: 01/11/2021 - 31/10/2024 Characterization of the CD8 T cell response in Parkinson’s disease for the development of preventive and therapeutic strategies that halt the progression of the disease: SARS-Cov-2-induced long term-hyposmia as a possible prodromal stage IP: Jordi Bove Badell Col·laboradors: Miquel Vila Bover, Alejandro Ferré Masó, Oriol de Fabregues-Boixar Nebot, Carles Lorenzo Bosquet, Thais Cuadros Arasa, Antonio Palasi Franco, David Ramos Vicente, Maria Sellés Altés Entitat finançadora: Instituto de Salud Carlos III Finançament: 165770 Referència: PI21/01358 Durada: 01/01/2022 - 31/12/2024 Paginació Pàgina actual 1 Page 2 Page 3 Page 4 Page 5 … Pàgina següent › Última pàgina »
