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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)

Institutions of which they are part

Head of group
Neurodegenerative Diseases
Vall Hebron Institut de Recerca
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

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



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: -

Ministerio de Ciencia

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
Funding agency: Michael J. Fox Foundation
Funding: 1269495.05
Reference: ASAP_MJFF2021
Duration: 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
Collaborators: Miquel Vila Bover, Alejandro Ferré Masó, Oriol de Fabregues-Boixar Nebot, Carles Lorenzo Bosquet, Thais Cuadros Arasa
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
Funding agency: Instituto de Salud Carlos III
Funding: 171820
Reference: PI21/01603
Duration: 01/01/2022 - 31/12/2024

Related news

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