Miquel Vila Bover I am an ICREA Professor and I lead the Research Group on Neurodegenerative Diseases at the Vall d'Hebron Research Institute (VHIR) Instituciones de las que forman parte Jefe de grupo Enfermedades Neurodegenerativas Vall Hebron Institut de Recerca Miquel Vila Bover Instituciones de las que forman parte Jefe de grupo Enfermedades Neurodegenerativas Vall Hebron Institut de Recerca I am an ICREA Professor and I lead the Research Group on Neurodegenerative Diseases at the Vall d'Hebron Research Institute (VHIR)
I have a degree in Medicine and Surgery from the University of Barcelona (1993) and a PhD in Neuroscience from the University of Paris 6 (1998). My doctoral work carried out in the laboratory of experimental neurology at the Salpetriere Hospital in Paris (1993-98) contributed to establishing the subthalamic nucleus as the main therapeutic target for the surgical treatment of Parkinson's disease with deep brain stimulation. From 1998 to 2005 I worked at the Movement Disorders Unit of Columbia University in New York (USA), initially as a postdoctoral researcher and from 2001 as an Assistant Professor of Neurology, focusing on the study of the mechanisms of neuronal death in Parkinson's disease to identify new therapeutic targets for this currently incurable neurodegenerative disorder. In 2006 I moved to Barcelona as a Professor at ICREA (Catalan Institute of Research and Advanced Studies) to create and lead a new research group in neurodegenerative diseases at the Vall d'Hebron Research Institute (VHIR). Our group is now part of the Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED) and the Aligning Science Across Parkinson's Collaborative Research Network (ASAP-CRN). I am also an Associate Professor at the Autonomous University of Barcelona, Principal Investigator at CIBERNED, Coordinating Lead PI at ASAP-CRN and member of the Steering Committees of the World Parkinson Coalition and the Basic Science Special Interest Group of the International Parkinson and Movement Disorder Society.
Líneas de investigación 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 Neuromelanin and Parkinson's disease In Parkinson's disease (PD), there is a selective degeneration of neurons that contain a dark-brown pigment called neuromelanin, especially dopaminergic neurons of the substantia nigra, which leads to the classical motor symptoms of the disease. However, the physiological significance of neuromelanin and its potential contribution to PD pathogenesis remain unknown. IP: Miquel Vila Bover Paginación Página actual 1 Página 2 Siguiente página › Última página » Proyectos Interacción patogénica entre la acumulación de neuromelanina y factores de susceptibilidad a la enfermedad de Parkinson: rol en el inicio y progresión de la enfermedad (NeuromelaninPD) IP: Miquel Vila Bover Colaboradores: Javier Hoyo Pérez, Gerard Roch Alba, Marta González Sepúlveda, Joana Margalida Cladera Sastre, Annabelle Parent Entidad financiadora: Ministerio Ciencia, Innovación y Universidades Financiación: 337500 Referencia: PID2024-159556OB-I00 Duración: 01/09/2025 - 31/08/2028 Neuromelanin and PD: mechanisms and therapeutic perspectives IP: Miquel Vila Bover Colaboradores: - Entidad financiadora: Michael J. Fox Foundation Financiación: 441200 Referencia: NEUROMELANIN-PD_M.VILA_MJFF2025 Duración: 01/07/2025 - 30/06/2027 Neurodegeneratives IP: Miquel Vila Bover Colaboradores: - Entidad financiadora: Fundació Institut de Recerca HUVH Financiación: 160000 Referencia: VILA/BOOST/2024 Duración: 15/11/2024 - 14/11/2028 Red de Investigación MitoNED: (Dis)función mitocondrial en enfermedades neurodegenerativas IP: Miquel Vila Bover Colaboradores: - Entidad financiadora: Ministerio de Ciencia e Innovación-MICINN Financiación: 0.01 Referencia: RED2022-134786-T Duración: 01/06/2023 - 31/05/2025 Paginación Página actual 1 Página 2 Página 3 Página 4 Página 5 … Siguiente página › Última página »
