Professor of Biochemistry and Molecular Biology since 2024 at the Faculty of Veterinary Medicine of the Complutense University of Madrid. He has a degree in Pharmacy from the Universidad Complutense de Madrid (1996) and did his PhD thesis in the laboratory of Prof. Miras-Portugal at the Faculty of Veterinary Medicine of the Universidad Complutense de Madrid, studying the molecular mechanisms through which purinergic receptors can modulate synaptic plasticity (2002).
After working in the laboratories of Prof. Voight at St. Louis University, USA in 2001 and in the laboratory of Prof. Soto at the Max-Planck-Institute in Göttingen, Germany in 2002, she started her postdoctoral stage in the laboratory of Prof. Lucas at the Centro de Biología Molecular Severo Ochoa (CBMSO) in October 2002. There he began to study the molecular mechanisms that are affected in different neurodegenerative diseases, starting with Huntington's disease (Díaz-Hernández et al., 2003, 2004 and 2005 J. Neurosci). With these roots, his scientific interest led him to question whether alterations in purinergic transmission could be one of the molecular mechanisms underlying neurodegenerative diseases. Thanks to a Juan de la Cierva contract (2005-2008) and later a Ramón y Cajal contract (2008-2009), he was able to develop his first studies to this end (Diaz-Hernández et al 2009, FASEB journal). Since 2009 he has been leading his own research group, whose main objective is to identify the molecular mechanisms underlying neurodegenerative processes in order to find new effective therapeutic strategies to combat these diseases. His group has pioneered the discovery of therapeutic effects of P2X7 antagonists in these pathologies, such as Alzheimer's disease (AD) (Diaz-Hernandez et al. 2010, JBC; DiazHernandez et al. 2012, Neurobiol Aging), Huntington's disease (Diazhernandez et al. FASEB 2009) taupathies (Di Lauro et al. 2021, Prog. Neurobiol), epilepsy (Engel et al., 2012 FASEB J). Likewise, their studies have shown that TNAP ectonuclease is also involved in pathological processes associated with AD (Sebastian-Serrano 2022 Neurobiol. Dis.) or epilepsy (Sebastian-Serrano et al. 2016, Hum Mol Genet). Finally, his results point out that other purinergic receptors, such as P2Y2R, could be good therapeutic targets to treat neuroinflammation associated with neurodegenerative processes (de Diego-Garcia et al. 2018 FASEB J). He has made more than 50 scientific publications, obtained 8 national and international funding, and participated in more than 90 congresses.