Esther Dalfó Capella

Esther  Dalfó Capella

Esther Dalfó Capella

Academic Staff

+34 935 811 624




Thesis number in address

1997: BS in Biology The University of Girona

1999: BS in   Biochemistry. Autonomous University of Barcelona (UAB, 1999).

MSc in Biochemistry and Molecular Biology. Mentors : Dra Mercedes Unzeta and Jose Miguel Lizcano. Autonomous University of Barcelona. School of Medicine

2004:  PhD in Biochemistry and Molecular Biology. Mentor: Dr Isidre Ferrer. School of Medicine.

2005 (Septmeber-December): Postodoctoral research fellow. Boston University Medical School. Department of Pharmacology. Boston, Massachusets, USA

2005-2007: Postodoctoral research fellow. Institute of Neuropathology, Bellvitge Institute of Biomedical Investigations(IDIBELL),  Barcelona.

2008-2009: Postodoctoral research fellow. Deaprtment of Bioinformatics and Molecualr genetics. Institute of Biology, Albert Ludwing Universty of Freiburg, Freiburg, Germany.

2010-2016: Miguel Servet Investigator, Bellvitge Institute of Biomedical Investigations(IDIBELL), Barcelona.

2016-2019: Adjunct Professor.  Autonomous University of Barcelona. School of Medicine .

2017-current: Associate Professor in basic medical sciences. Universitat de Vic-Universitat Central de Catalunya. Faculty of Medicine.

2016-current: Group leader of C elegans models of human diseases, Institut de Neurociències, UAB.

She is a principal investigator at the Signaling and New Therapeutic Targets (SINDATER)

We are interested in deciphering the molecular metabolic mechanisms associated with neurodegenerative diseases, mainly in Parkinson's Disease (PD) related disorders. The death of dopaminergic (DA) neurons in the substantia nigra pars compacta of the brain is responsible for the motor disability characterizing the disease. The main histopathological hallmark of PD is abnormal accumulation and aggregation of intracellular a-synuclein (Asyn) in the form of Lewy Bodies (LB) in DA neurons. These aggregates constitute the hallmark of a group of diseases called synucleinopathies. In this scenario, we discovered a role of the parkin gene, mutated in some familiar variants of PD, in the engulfment of apoptotic cells in C elegans. Concretely, parkin modulates the expression and activity of the small GTPase Rac1, which plays an essential role in celular citoskeleton. Interestingly, we demonstrated that Rac1 function is essential in the modulation of DA cell death induced by Asyn. We are now investigating the mechanisms by which Rac1 function participates in the development of PD. Our main stategy is focused on investigating the lipidomic fingerprint of Rac1 in the pathogenesis of PD, by using C elegans as the main tool of our research.
The main goal of my lab is to translate basic sicence to medical and therapeutic applications for contributing to the understanding, prevention and cure of neurodegenerative diseases.

  • The Small GTPase RAC1/CED-10 Is Essential in Maintaining Dopaminergic Neuron Function and Survival Against α-Synuclein-Induced Toxicity. Kim H, Calatayud C, Guha S, Fernández-Carasa I, Berkowitz L, Carballo-Carbajal I, Ezquerra M, Fernández-Santiago R, Kapahi P, Raya Á, Miranda-Vizuete A, Lizcano JM, Vila M, Caldwell KA, Caldwell GA, Consiglio A, Dalfo E. Mol Neurobiol. 2018 Sep;55(9):7533-7552. doi: 10.1007/s12035-018-0881-7. Epub 2018 Feb 10. 
  • PDR-1/hParkin negatively regulates the phagocytosis of apoptotic cell corpses in Caenorhabditis elegans. Cabello J, Sämann J, Gómez-Orte E, Erazo T, Coppa A, Pujol A, Büssing I, Schulze B, Lizcano JM, Ferrer I, Baumeister R, Dalfo E. Cell Death Dis. 2014 Mar 13;5:e1120. doi: 10.1038/cddis.2014.57.


Institut de Neurociències
Tel: 93 581 3861 / Fax: +34 93 581 3327

Facultat de Medicina. Edifici M-1
Avinguda de Can Domènech - Campus de la UAB · 08193
Bellaterra (Cerdanyola del Vallès) · Barcelona