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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

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

Identification of biomarkers of prodromal Parkinson's disease

Despite intensive efforts towards understanding the aetiology/pathogenesis of Parkinson's disease (PD) and the development of novel therapeutic approaches for this neurodegenerative condition, the current treatment for PD remains symptomatic and yet far from modifying disease onset or progression. Before the manifestation of the classical motor symptoms, PD patients present with non-motor symptoms in a prodromal phase. The identification of deregulated molecular pathways or genes in peripheral blood and/or cerebrospinal fluid from these prodromal patients may help develop potential biomarkers for the early detection, diagnosis, risk assessment and/or progression of PD, which are currently lacking, as well as to stratify patients at very early stages to apply more specific, personalized disease-modifying treatments.

IP: Miquel Vila Bover, Ariadna Laguna Tuset

Proyectos

Neuromelanin and PD: mechanisms and therapeutic perspectives

IP: Miquel Vila Bover
Colaboradores: -
Entidad financiadora: Michael J. Fox Foundation
Financiación: 441200
Referencia: MJF/NETWORKS/2024/VILA
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

Ministerio de Ciencia

Malalties neurodegeneratives

IP: Miquel Vila Bover
Colaboradores: Jorge Hernández Vara, Malalties neurodegeneratives , Marta Martínez Vicente, Jordi Bove Badell, Eddie Pradas Gracia, Maria Camprodon Gomez, Laura Castillo Ribelles, Oriol de Fabregues-Boixar Nebot, Javier Hoyo Pérez, Ariadna Laguna Tuset, Maria Sellés Altés, Marta González Sepúlveda, Joana Margalida Cladera Sastre, Annabelle Parent, Daniela Samaniego Toro, Malalties neurodegeneratives
Entidad financiadora: Agència Gestió Ajuts Universitaris i de Recerca
Financiación: 40000
Referencia: 2021 SGR 00784
Duración: 01/01/2022 - 30/06/2025

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