Miquel Vila received his MD from the University of Barcelona (Spain) and then moved to the laboratory INSERM U289 (Prof. Y. Agid) at the Salpêtrière Hospital (Paris, France), where he obtained a Master degree (DEA) and PhD in Neuroscience from the University of Paris 6. From 1998 to 2001 he worked as a postdoctoral researcher at the laboratory of Dr. S. Przedborski at the Dept. of Neurology of Columbia University (New York, USA). In 2001, he obtained a tenure-track position as Assistant Professor of Neurology at Columbia University, a $1M-R01 NIH grant and the US permanent residency (outstanding researcher category). In December 2005, he moved back to Barcelona as an ICREA Research Professor to create and lead a new research group on Neurodegeneration at the Vall d'Hebron Research Institute, with the support of a 1.5M€ European Commission's Marie Curie Excellence Grant. He also holds positions as Associate Professor at the UAB and as Principal Investigator at the CIBERNED.
Our research is geared toward elucidating the molecular mechanisms of neuron cell death occurring in Parkinson’s disease, the second most common neurodegenerative disorder after Alzheimer’s dementia, in order to: (i) identify biomarkers for the diagnosis, early detection, patient stratification, disease progression, prognosis or response to treatment, (ii) identify new molecular targets for potential therapeutic intervention, (ii) develop novel therapeutic strategies with disease-modifying potential for this currently incurable disease, (iv) unravel molecular pathways common to other neurodegenerative diseases.
– Carballo-Carbajal I, Laguna A, Romero-Gimenez J, Cuadros T, Bové T, Martinez-Vicente M, Parent A, Gonzalez-Sepulveda M, Peñuelas N, Torra A, Rodriguez-Galvan B, Ballabio A, Hasegawa T, Bortolozzi A, Gelpi E & Vila M 2019 ‘Brain tyrosinase overexpression implicates age-dependent neuromelanin production in Parkinson’s disease pathogenesis‘. Nature Communications, volume 10, 973.
– Vila M 2019, ‘Neuromelanin, aging, and neuronal vulnerability in Parkinson’s disease’, Movement Disorders, 34(10): 1440-1451.
– Vila M, Laguna A & Carballo-Carbajal I 2019, ‘Intracellular crowding by age-dependent neuromelanin accumulation disrupts neuronal proteostasis and triggers Parkinson disease pathology’, Autophagy, 15, 11, 2028 – 2030.