José Lucas - Biography#

Prof. Lucas has coined outstanding advances on the etiology and therapeutics of neural disease.

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).

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.

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).

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).

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).