Sergio Barlati
Sergio Barlati
affiliation: Università di Brescia
research area(s): Genetics And Genomics, Neuroscience
Course: Molecular Genetics, Biotechnologies and Experimental Medicine
University/Istitution: Università di Brescia
short CV of Sergio Barlati

- Full Professor of Biology and Genetics at the Medical Faculty ,University of Brescia (UNIBS).
- Director of Research Centre on Hereditary Disorders;
- Coordinator of PhD Program in Molecular Genetics;
-Director of the Laboratory of Cytogenetics and Molecular Genetics (LCGM) of the National Health Service of Lombardy Region (Italy).
From 1970 to 1982 at the Institute of Genetics, University of Pavia (Chairman Prof. Luigi L. Cavalli-Sforza), as Responsible of “Cell Culture Division”.
International experience:
From 1966 to 1969 PhD program at the Genetics Department, Stanford University, California, U.S.A with Prof. Joshua Lederberg (Nobel Laureate) working on Bacterial Genetics
Between 1970-1976, for two years, at the Fondation Curie in Paris, France collaborating with Dr. Philippe Vigier working on factors favouring cellular transformation and RNA oncoviruses.
From1978-1982, for about one year, at the Department of Virology of the University of Helsinki, Finland working on Fibronectin (FN) and FN fragments in collaboration with Prof. Antti Vaheri.
Administrative experience:
From 1990-1995 and 2002-2009 Chairman of the Department DSBB-UNIBS. Rector’s Delegate for International Affairs until 2010.
Scientific activity:
Author of more than 200 international publications (162 in PubMed).
Member of the: - Human Genome Organisation (HUGO); - American Society for Biochemistry and Molecular Biology (ASBBM); -Italian (SIGU) and European Society of Human Genetics (ESHG). Academy for Multidisciplinary Neurotraumatology (AMN)
Present research interests:
1) Genomic analysis of neurological disorders;
2) Development of software for genome analysis
3) Molecular biology/genetics of spinal cord injury
4) Glutamate receptors and molecular neurobiology;
5) Molecular genetics and hereditary disorders.
1. Caracciolo L, Barbon A, Palumbo S, Mora C, Toscano CD, Bosetti F, Barlati S. (2011). Altered mRNA editing and expression of ionotropic glutamate receptors after kainic Acid exposure in cyclooxygenase-2 deficient mice. PLoS One. May 12;6(5):e19398.
2. Russo I, Barlati S, Bosetti F. (2011). Effects of neuroinflammation on the regenerative capacity of brain stem cells. J Neurochem. ;116(6):947-56.
3. Magri C, Sacchetti E, Traversa M, Valsecchi P, Gardella R, Bonvicini C, Minelli A, Gennarelli M, Barlati S. (2010). New copy number variations in schizophrenia. PLoS One. 13;5(10):e13422.
4. Francolini M, Brunelli G, Cambianica I, Barlati S, Barbon A, La Via L, Guarneri B, Boroni F, Lanzillotta A, Baiguera C, Ettorre M, Buffelli M, Spano P, Clementi F, Pizzi M. (2009). Glutamatergic reinnervation and assembly of glutamatergic synapses in adult rat skeletal muscle occurs at cholinergic endplates. J . Neuropathol Exp Neurol. ;68(10):1103-15.
5. Fiorini M, Piovani G, Schumacher RF, Magri C, Bertini V, Mazzolari E, Notarangelo L, Notarangelo LD, Barlati S. (2009). ITGB2 mutation combined with deleted ring 21 chromosome in a child with leukocyte adhesion deficiency. J Allergy Clin Immunol.124(6):1356-8.
6. Barlati S, Chiesa S, Magri C. (2009) "GenotypeColour": colour visualisation of SNPs and CNVs. BMC Bioinformatics. 10:49.
7. Magri C, Gardella R, Valsecchi P, Barlati SD, Guizzetti L, Imperadori L, Bonvicini C, Tura GB, Gennarelli M, Sacchetti E, Barlati S. (2008). Study on GRIA2, GRIA3 and GRIA4 genes highlights a positive association between schizophrenia and GRIA3 in female patients. Am J Med Genet B 5;147B(6):745-53.
8. Drera B, Barlati S, Colombi M. (2007) Ischemic stroke in an adolescent with arterial tortuosity syndrome.
Neurology. 2007 May 8;68(19):1637;
9. Pizzi M, Brunelli G, Barlati S, Spano P. (2006). Glutamatergic innervation of rat skeletal muscle by supraspinal neurons: a new paradigm in spinal cord injury repair. Curr Opin Neurobiol. 16(3):323-8.
10. Coucke PJ, Willaert A, Wessels MW, Callewaert B, Zoppi N, De Backer J, Fox JE, Mancini GM, Kambouris M, Gardella R, Facchetti F, Willems PJ, Forsyth R, Dietz HC, Barlati S, Colombi M, Loeys B, De Paepe A. (2006). Mutations in the facilitative glucose transporter GLUT10 alter angiogenesis and cause arterial tortuosity syndrome. Nat Genet.38(4):452-7.
11. Magri C, Gardella R, Barlati SD, Podavini D, Iatropoulos P, Bonomi S, Valsecchi P, Sacchetti E, Barlati S. (2006). Glutamate AMPA receptor subunit 1 gene (GRIA1) and DSM-IV-TR schizophrenia: a pilot case-control association study in an Italian sample. Am J Med Genet B 5;141B(3):287-93.
12. Barbon A, Popoli M, La Via L, Moraschi S, Vallini I, Tardito D, Tiraboschi E, Musazzi L, Giambelli R, Gennarelli M, Racagni G, Barlati S. (2006). Regulation of editing and expression of glutamate alpha-amino-propionic-acid (AMPA)/kainate receptors by antidepressant drugs. Biol Psychiatry. 15;59(8):713-20
Project Title:
The analysis the DNA obtained from controls and patients affected by complex neurological and behavioral disorders, using Affymetrix array for the evaluation of SNP and CNV, led to the identification of several genes that might be involved in the pathology under study. The parallel development of specific software, for the evaluation of the of genomic data obtained, and the extension of the analysis to family study, should led to the elucidation of specific functional pathway that might favor the appearance of the pathology.
This data, in combination with parallel molecular studies on the neuronal cells obtained from the embryonic brains of experimental animals, should complement the result obtained and add information on the ethiopatogenesis of the specific neuronal disorders

Project Title:
The analysis of the mRNA and proteins coding for the different types of ionotropic glutamate receptors subject to mRNA editing will be performed on mice and rat neuronal embryonic cell cultures in order to evaluate their localization and function. The mRNA location of the different GLUR isophorms in relationship with editing levels will be studied as a function of differential neuronal stimulation and knock out of specific genes.