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) Institutions of which they are part Head of group Neurodegenerative Diseases Vall Hebron Institut de Recerca Email Miquel Vila Bover Email Institutions of which they are part Head of group Neurodegenerative Diseases 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.
Research lines 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 Pagination Current page 1 Page 2 Next page › Last page » Projects Red de Investigación MitoNED: (Dis)función mitocondrial en enfermedades neurodegenerativas IP: Miquel Vila Bover Collaborators: - Funding agency: Ministerio de Ciencia e Innovación-MICINN Funding: 0.01 Reference: RED2022-134786-T Duration: 01/06/2023 - 31/05/2025 Malalties neurodegeneratives IP: Miquel Vila Bover Collaborators: Jorge Hernández Vara, Joan Compte Barrón, Marta Martínez Vicente, Jordi Bove Badell, Eddie Pradas Gracia, Maria Camprodon Gomez, Malalties neurodegeneratives , 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, Helena Xicoy Cortada, Alba Nicolau Vera, Marta González Sepúlveda, Joana Margalida Cladera Sastre, Annabelle Parent, Daniela Samaniego Toro, Daniela Samaniego Toro Funding agency: Agència Gestió Ajuts Universitaris i de Recerca Funding: 40000 Reference: 2021 SGR 00784 Duration: 01/01/2022 - 30/06/2025 MECANISMOS MOLECULARES DE NEURODEGENERACION LIGADA A LA NEUROMELANINA EN LA ENFERMEDAD DE PARKINSON Y ENVEJECIMIENTO CEREBRAL IP: Miquel Vila Bover Collaborators: Gerard Roch Alba, Miriam Izquierdo Sans Funding agency: Ministerio de Ciencia e Innovación-MICINN Funding: 99260 Reference: PRE2021-098300 Duration: 01/07/2022 - 30/06/2026 Activity and connectivity drive neuronal vulnerability and disease progression in Parkinson's disease IP: Miquel Vila Bover Collaborators: Joan Compte Barrón, Javier Hoyo Pérez, Gerard Roch Alba, Marta González Sepúlveda, Ariadna Laguna Tuset, Joana Margalida Cladera Sastre Funding agency: Michael J. Fox Foundation Funding: 1269495.05 Reference: ASAP_MJFF2021 Duration: 01/11/2021 - 31/10/2024 Pagination Current page 1 Page 2 Page 3 Page 4 Page 5 … Next page › Last page »
