Andréa Laurato Sertié curriculum
Date of Birth: 12/10/1972
Citizenship: Brazilian
Language Fluency: English
Address:
Department of Psychiatry, Faculty of Medicine - University of São Paulo
P.O. Box 8091
05403-010
São Paulo - SP – Brazil
Telephone +5511 3069.7283; Telefax: +5511 3062.9029
e-mail: asertie@hotmail.com
Academic Degree
PhD Molecular Biology – Human Genetics
Education
1991-1995: College/University: Bachelor degree in Biosciences, Biosciences Institute, University of São Paulo, Brazil
1995-2000: PhD in Molecular Biology – Human Genetics, Biosciences Institute, University of São Paulo, Brazil
2000-2002: Postdoctoral Fellow, Department of Developmental Biology, The Hospital for Sick Children, Toronto, Canada
2003-2007: Postdoctoral Fellow, Department of Genetics and Evolutive Biology, Biosciences Institute, University of São Paulo, Brazil
2008-present: Research scientist, Department of Psychiatry, Faculty of Medicine, University of São Paulo, Brazil
Professional experience
Human molecular genetics; Disease gene mapping; Functional characterization of gene function within neural circuits; Genome wide gene expression profiling; Molecular aspects of craniofacial dysmorphology; Stem cell biology; Pharmacogenomics
Current Research Projects
1. “Pharmacogenomic study of weight gain in schizophrenic patients treated with clozapine or olanzapine”.
Description: Second-generation antipsychotics (SGAs) are increasingly replacing the conventional antipsychotics used for the treatment of schizophrenia and other psychoses because of their excellent antipsychotic efficacy in the absence of extrapyramidal side effects. Unfortunately, patients treated with SGAs are also more likely to present with obesity, insulin resistance, dyslipidemia, abnormal glucose tolerance, and overt diabetes. It is clear that these side effects can undermine compliance, inclining patients to relapse, and may also lead to significant psychological distress and medical morbidity and mortality. Among the SGA, clozapine and olanzapine induce the most significant weight gain. It has been suggested that the weight gain and the metabolic adverse effects induced by SGAs are mediated by a central action, perhaps through the modulation of serotoninergic/noradrenergic pathways in the central nervous systems. It has also been recently shown that the SGAs exert direct cellular effects on insulin action and substrate metabolism in adipocytes, as well as stimulate neo-formation of adipocyte tissue. However the underlying mechanisms are unknown. Here we will utilize primary cultured human pre-adipocytes from schizophrenic patients who gained excessive weight during antipsychotic treatment to investigate molecular and cellular mechanisms by which chronic antipsychotic treatment alter adipogenic differentiation and metabolism.
2. “Dissection of the roles of collybistin, a neuron-enriched GDP-GTP exchange factor, in synapse formation and function”.
Description: The collybistin protein belongs to the GEF (guanine nucleotide exchange factors) family, which activates small Rho-like GTPases. Collybistin specifically actives Cdc42 GTPase in fibroblasts, promoting the reorganization and polarization of the actin cytoskeleton. In addition, collybistin interacts directly with the gephyrin protein and is responsible for the localization of gephyrin and glycine and GABAA receptors at the inhibitory postsynaptic membrane of neurons. Mutations in the human collybistin gene (ARHGEF9) were identified in three patients with neurological and behavioral abnormalities, including mental retardation, epilepsy, hyperekplexia, anxiety and aggression. Although these findings reveal that collybistin is an important determinant of inhibitory synapse formation and function, our understanding about it functions is far from complete. For instance, what are the additional collybistin binding partners?; does collybistin play other roles in neurons?; how collybistin is regulated?; how is the collybistin expression pattern in human brain? is collybistin involved in neurons cytoskeleton remodeling and in other neuronal diseases?. Therefore, our major aims are to dissect the role of collybistin in the protein network that governs inhibitory synapses formation and function and to analyse the involvement of ARHGEF9 in the patophysiology of hyperekplexia and epilepsy associated with mental retardation.
Scientific productivity
