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 Pagination First page « Previous page ‹ Page 1 Current page 2 Projects 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 Collaborators: Miquel Vila Bover, Alejandro Ferré Masó, Oriol de Fabregues-Boixar Nebot, Carles Lorenzo Bosquet, Thais Cuadros Arasa, Antonio Palasi Franco, David Ramos Vicente Funding agency: Instituto de Salud Carlos III Funding: 165770 Reference: PI21/01358 Duration: 01/01/2022 - 31/12/2024 The brain-body axis in Parkinson’s disease patients: from pathophysiology to biomarkers and therapeutic approaches IP: Ariadna Laguna Tuset Collaborators: Maria Victoria Gonzalez Martinez, Miquel Vila Bover, Marina Lorente Picón, Helena Xicoy Cortada, Daniela Samaniego Toro, Daniela Samaniego Toro, Sara Belmonte Calderon Funding agency: Instituto de Salud Carlos III Funding: 171820 Reference: PI21/01603 Duration: 01/01/2022 - 31/12/2024 NIPARK Neuromelamina como diana terapéutica en la enfermedad de Parkinson y envejecimiento cerebral: abordaje por neuroimagen y estimulación cerebral IP: Miquel Vila Bover Collaborators: Alba Nicolau Vera, Thais Cuadros Arasa, Marta González Sepúlveda Funding agency: Instituto de Salud Carlos III Funding: 249984.79 Reference: AC20/00121 Duration: 01/01/2021 - 31/12/2024 Characterization of a novel neuromelanin-producing transgenic mouse model: relevance to Parkinson's disease and brain aging IP: Miquel Vila Bover Collaborators: - Funding agency: Michael J. Fox Foundation Funding: 165760.76 Reference: NEUROMELANINE_MJFF2019 Duration: 13/12/2019 - 15/06/2022 Pagination First page « Previous page ‹ Page 1 Current page 2 Page 3 Page 4 Page 5 … Next page › Last page »
