I am a ​Marie Sklodowska-Curie Postdoc Fellow currently working at the Institute for Neuropathology at the University Medical Center Hamburg-Eppendorf (UKE) in Germany.

I am originally from Catalonia, where I performed my Bachelor's in Biology and Master's in Neuroscience at the University of Barcelona. Afterward, I did my Ph.D. at the Institute for Bioengineering of Catalonia, also in Barcelona. Under Prof. José Antonio del Río's supervision, my thesis focused on the pathophysiological role of the Prion protein (PrP) in the central nervous system. On one side, we developed the first iPSC model from a patient with a familiar Prionopathy related to a PrP mutation. In this work, we reproduce a common comorbid pathology associated with this disease, the Tauopathy, postulating PrP as a modulator of pathological Tau phosphorylation. In the project's second part, we described PrP's neuroprotective role in epilepsy, performing kainate-based epileptogenic models in vitro and in vivo with different mice models. Finally, we went further, characterizing the effects of PrP deficiency in mice behavior, memory, and hippocampal connectivity, combining in vitro calcium imaging and hippocampal electrophysiology recordings of awake mice. We also performed behavioral tests to define the consequences of PrP absence in learning and memory acquisition. With this overall approach, we describe PrP as a stabilizing protein that maintains synaptic integrity, regulates the maturation of neural connectivity, and is necessary for the proper response to excitatory insults. 

Now, my MSCA project, entiled: The role of extracellular vesicles in Alzheimer’s Disease: towards obtaining mechanistic insights to intrinsic protection mechanisms (H2020_MSCA-IF_2020-101030402_EXOSOMES_AD), is focused on the role of extracellular vesicles (EV) in Alzheimer's Disease. EVs have been shown to trap Aβ, which reduces Aβ-free oligomers load and Aβ-mediated toxicity, thereby exerting neuroprotective functions. Conversely, EVs also enhance the propagation of Aβ and Tau aggregates, thus promoting disease progression. Combining multi-omic analysis and in vitro iPSC-AD models, we describe the AD-EVs composition and the main protein actors in their seemingly dual role in AD, mainly focusing on the PrP and its role in Aβ aggregation/spreading.