Àlex Bayés (AB) received his PhD on Biochemistry in 2005 (UAB, Barcelona). His doctoral research dealt with structural, functional and evolutionary studies of pests proteases and their inhibitors. This research turned into eight publications including and article in PNAS (Bayés et al. PNAS 2005). In 2006 AB moved to the Sanger Institute (Cambridge, UK) where he performed a postdoctoral stay of over five years with Professor Seth GN Grant. There he started his career in neurosciences, working on the study of the molecular basis of synaptic function. Research during these years focused on the proteomic study of the postsynaptic protein complexes found at glutamatergic synapses. He focused in two main complexes: the postsynaptic density (PSD) and the signalling complex associated to PSD95 and its family members. These complexes contain hundreds of different proteins (especially the PSD) including all the key molecules involved in the reception and integration of the neural signal. AB uses systems biology tools, mainly proteomics and bioinformatics, to study the synaptic proteome. His methodology arouses from the notion that the synapse, and particularly the PSD, is a highly coordinated molecular machines, which has to be studied as a whole. This experimental approached was outlined in the following publication: Bayés A and Grant SG. Nature Reviews Neuroscience. 2009. AB research on the postsynaptic proteome focused on its evolution and its role in central nervous system diseases. Evolutionary studies showed that synaptic proteomic complexity has not grown gradually through animal evolution, but actually doubled twice, in the transition from organisms without nervous system to invertebrates, and from invertebrates to vertebrates (Emes et al. Nat. Neuroscience 2008). Furthermore, his work showed that within mammals the genes that constitute the PSD have been under a very strong evolutionary constraint, being the most conserved of all genes expressed in human neurons (Bayés et al. Nat Neuroscience 2011). AB work has also exposed the very high compositional similarity of the postsynaptic proteome across all vertebrates (Bayés et. al. Nat. Communications. 2017; Bayés et. al. PLoS ONE 2012). AB research on the relevance of the PSD in disease identified more than 130 central nervous system diseases caused by genes expressed at the PSD. These covered a wide range of disease types, including common neurodegenerative diseases (Alzheimer’s, Parkinson’s, Huntington’s), adult and childhood mental and behavioural disorders, motor disorders such as ataxia or dystonia, epilepsies and many rare diseases. AB discovered that the number of genes expressed in the human PSD causing disease was disproportionately high, suggesting that the PSD is highly relevant to brain dysfunction (Bayes et al. Nat Neuroscience 2011). Finally AB research identified that the PSD is particularly relevant to diseases causing cognitive dysfunction, such as Intellectual Disability (ID) and Schizophrenia (Kirov et al. Mol. Psychiatry 2012). AB work has also dealt with developing standards and methods to perform synapse biochemistry and proteomics with human post-mortem tissue (Bayes et al. Mol Brain 2014). In may 2012 AB established his own laboratory in the Biomedical Research Institute Sant Pau, where he is now a fully appointed Group Leader, working with animal models of ID caused by genes expressed specifically at the PSD (SYNGAP1 and SHANK2) in order to understand the synaptic molecular pathology behind these disorders.