!!José Lucas - Biography
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Prof. Lucas has coined outstanding advances on the etiology and therapeutics of neural disease.\\
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His PhD stage (1990-1993) at Cajal Institute (Madrid) yielded important advances on the molecular basis of pain regulation (Oncogene 6:223-7 1991; Neuron 10:599-611 1993). As postdoctoral fellow at Columbia University (N. York) (1994-1998) he unveiled molecular clues of addiction in the 5-HT1B receptor-KO mouse model (Mol Pharmacol 51:755-763, 1997 and Nature 393:175-178, 1998).\\
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In 1998 he moved to CBMSO (Madrid) where he was appointed Tenured Scientist in 2000 and Research Professor in 2008, he is also CIBERNED-Principal Investigator.\\
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He was the first to demonstrate that neurodegenerative diseases are susceptible to revert by generating the first conditional mouse mode of one of these diseases, namely Huntington (Cell 101:57-66, 2000; cited 769 times). The conditional mouse model of Alzheimer disease by GSK-3 overexpression (EMBO J 20:27-39, 2001; cited 681 times) allowed to consolidate GSK-3 as a therapeutic target and he also explored ways to facilitate the use of GSK-3 inhibitors such as lithium for Alzheimer and bipolar disorder (EMBO J 26:2743-54, 2007 and J Clin Invest 120:2432-45, 2010). \\
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Regarding Huntington's pathogenesis, he has characterized in-depth the ubiquitin-proteasome system (UPS) and the endoplasmic reticulum stress (ERS) (J Neurosci 23:11653-61, 2003, Trends Neurosci 27:66-70 2004, PNAS 106:13986-91 2009, J Neurosci 30:3675-88 2010, Brain 136:577-92 2013 and Brain 136:1161-76, 2013). Later, he reported alteration of the splicing machinery in Huntington leading to a toxic role of tau protein and discovered a new histopathological hallmark: the Tau Nuclear Rods. (Nat Med 20:881-5, 2014-highlighted in Nat Rev Neurosci 15:564, 2014).\\
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By studying cytoplasmic polyadenylation in Huntington he recently discovered a new regulator of Autism risk gene expression -CPEB4- which links autism genetics with the underlying environmental factors (Nature 550:441-6, 2018).\\ \\