Asset 2 Conferences
Chávez Gutiérrez, Lucía - profile picture

Lucía Chávez Gutiérrez

VIB Center for Brain and Disease Research, BE
Biography

Lucía Chávez-Gutiérrez (LCG) holds a PhD in Sciences with a major in Biochemistry from the National University of Mexico.

Trained as biochemist with a strong background in enzymology and protein structure, LCG studies proteolytic mechanisms and their (dys)regulation on the premise that developing a solid mechanistic understanding will offer critical insights into how these molecular switches control fundamental cellular processes in physiology and disease.

Her fascination for proteases and the connection with brain function and disease motivated her postdoctoral studies in the laboratory of Prof. Bart De Strooper, where she investigated the γ-secretase intramembrane proteases and their pathogenic involvement in Alzheimer‘s disease.

Early-onset familial Alzheimer’s disease (FAD) is caused by mutations in Presenilin (PSEN, catalytic subunit of the γ-secretase proteases) and the Amyloid Precursor protein (APP). The studies of LCG settled down a long-standing “Loss-of-function vs. Gain-of-function” debate on the aetiology of FAD (Chávez-Gutiérrez et al, EMBO 2012; Szaruga et al, JEM 2015 and Veugelen et al, Neuron 2016) by demonstrating that pathogenic mutations in Presenilin variably affect the overall activity of γ-secretase -which controls key signalling cascades- but invariably increase the production of longer, aggregation-prone Aβ peptides.

Her mechanistic and genetically-led work has shown that the enhanced generation of longer Aβ species arises from the mutation-driven destabilizing effects on γ-secretase-APP interactions (Szaruga et al, Cell 2017). These mechanistic findings placed Aβ at the core of Alzheimer‘s pathogenicity and support the stabilization of γ-secretase-APP interactions (Petit et al EMBO J 2019) as a potential therapeutic strategy.

Speaker at

OC member at