Paola Sgadò

• 25th Sept 2006          PhD awarded “magna cum laude” - University of Heidelberg, Germany. Title: “Development and maintenance of mesencephalic dopaminergic neurons: role of the Engrailed and Pbx1 transcription factors”. Supervisors: Prof. K. Beyreuther and Prof. H. Monyer.
• 26th April 1999         Master in Biological Science – Graduation with honour “110/110 cum laude”, at the University of Pisa, Italy. Thesis: “PC3 over-expression, driven in vivo by retroviral vectors, affects terminal differentiation of rat cortical precursors”. Supervisor Dr. F. Cremisi., Scuola Normale Superiore, Pisa.

• Jan 2022 – present   Researcher (type B) in Physiology (BIO/09) – Center for Mind/Brain Sciences (CIMeC) – Unversity of Trento
• Jan 2017 – Jan 2022   Researcher (type A) in Physiology (BIO/09) – Center for Mind/Brain Sciences (CIMeC) – Unversity of Trento
• Jan 2017 – present   Head of the Molecular and Cellular Cognition (mc2) group – Animal Cognition and Neuroscience Lab – Center for Mind/Brain Sciences (CIMeC)
• Jan 2017 – Apr 2019   Member of the PhD Committee in “Cognitive and Brain Sciences” – Univerity of Trento, Rovereto TN Italy.
• Jul ’15 – Dec ’16       Senior PostDoc at the Animal Cognition and Neuroscience Laboratory, Center for Mind/Brain Science, University of Trento, Italy.
• Jul ’10 – Dec ‘14       Marie Curie COFUND “People” Incoming PostDoc 2009 Research Fellow. EnCORT Project [149.000 €]. Centre for Integrative Biology (CIBIO), University of Trento, Italy.
• Aug ’10 – Jun ’11     Maternity leave
• Jun ’09 – Jun ’10      Senior PostDoc in Laboratory of Molecular Neuropathology, Centre for Integrative Biology (CIBIO), University of Trento, Italy.
• Jun ’07 – May ’09     PostDoc in Neurogenentics of Epilepsy at the Neurogenetics lab, Child Neurology Unit, “A. Meyer” Children’s Hospital, Florence, Italy.
• May ’05 – Apr ’07     PostDoc at the Neuroscience Department, Pharmacology section, University of Pisa, Italy.
• 25th Sept 2006          PhD awarded “magna cum laude” - University of Heidelberg, Germany. Title: “Development and maintenance of mesencephalic dopaminergic neurons: role of the Engrailed and Pbx1 transcription factors”. Supervisors: Prof. K. Beyreuther and Prof. H. Monyer.
• Feb ’00 – Dec ’04      PhD student under the supervision of Dr. Horst Simon, at the Interdisciplinary Centre for Neuroscience, Department of Neuroanatomy III, University of Heidelberg, Germany.
• Apr ’99 – Feb ’00      Research assistant in Developmental Biology at the Cellular and Developmental Biology Lab, Biochemistry and Physiology Department, University of Pisa, Italy. Supervisor: Dr. F. Cremisi.
• 26th April 1999         Master in Biological Science – Graduation with honour “110/110 cum laude”, at the University of Pisa, Italy. Thesis: “PC3 over-expression, driven in vivo by retroviral vectors, affects terminal differentiation of rat cortical precursors”. Supervisor Dr. F. Cremisi., Scuola Normale Superiore, Pisa.
• Apr ’96 – Apr ’99      Undergraduate research training at the Cellular and Developmental Biology Lab, Biochemistry and Physiology Department, University of Pisa, Italy.
• Nov ’92 – Apr ’99     Master Degree Course in Biological Science, University of Pisa, Italy.

My research aims at exploring the effect of ASD-related alterations (both pharmacological and genetical) on the development of social skills in domestic chicks, and in particular on the study of social predispositions, early social-orienting mechanisms emerging in the first hours after birth in humans as well as domestic chicks. We found that VPA, an anticonvulsant previously shown to increase the risk of ASD, changes the chicks’ early-social orienting mechanisms, without affecting basic brain functions, such as motor control and filial imprinting. We are currently broadening the study of social predispositions affected by VPA and analyzing the neurobiological bases of these deficits, to identify relevant brain areas, neurotransmitter systems and molecular pathways necessary for the expression of social predispositions in chicks. To my knowledge the chick VPA model is the first to link ASD-relevant behavioral deficits induced by VPA with behavioral task that are analogous to human social behavior. We are also developing gene editing strategies in domestic chicks to induce gene alterations relevant for ASD and test the effect of ASD-associated gene mutation on the development of social-orienting mechanisms in domestic chicks. 

We believe that the study of the brain circuits and the gene networks involved in social predispositions in chicks, and affected by ASD- inducing pharmacological or genetic manipulations, may potentially shed light on the earliest disturbances and the neurobiological bases of ASD. Using this novel class of inter-species social-orienting mechanisms and ASD-modelling in domestic chicks, we believe we present a new tool of potential translational value to investigate the mechanistic bases of ASD social deficits with the aid of early behavioural markers analogous to those used in human studies. 

Jan’17 – present Principal Investigator at the Molecular and Cellular Cognition (mc²) group investigating the molecular and cellular components of cognitive processes. The research is mainly focused on the molecular bases of social cognition and their link to neurodevelopmental disorders, using a combination of behavioural, neurobiological and molecular techniques.

Jul ’15 – Dec ’16 PostDoc research experience on “Neurobiological bases of animal behaviour” at the Centre for Mind/Brain Science, University of Trento. The research aimed to study the neurobiological mechanisms underlying animal behavior using a combination of behavioural and neurobiological technique such as the expression of immediate early genes, electrophysiology, anatomy and molecular genetics.

Jul ’10 – Dec ’14 Marie Curie COFUND Incoming PostDoc 2009; EnCORT Project. Project title: “Neurodevelopmental bases of ASD: cortical inhibitory system development in En2 knockout mice” at the Centre for Integrative Biology, University of Trento. The project aimed at analysing the effect of En2 mutation in the development of GABAergic interneurons. We found a significant loss of PV interneurons in the sensory cortices of En2 mutants already at postnatal day 10, accompanied by molecular alterations in the expression of ASD-related genes (Fmr1, mGluR5, BDNF and KCC2). Data suggest delayed maturation of cortical circuits in En2 mice and altered sensory processing and integration in these mice. Moreover, our transcriptome analysis revealed that En2 regulates a complex network of ASD-related genes, confirming and expanding the idea that ASD results from alterations of conserved transcriptional pathways.

Jun ’09 – Jun ’10PostDoc research experience on “Neuroanatomical characterization of the En2 knock-out mice, a model for autistic spectrum disorders” at the Molecular Neuropathology lab, Centre for Integrative Biology, University of Trento, (Head Dr. Y. Bozzi). The project involved the set up a new research line regarding the characterization of En2 mutant phenotype in the forebrain. The results strengthen the hypothesis of a prominent role of GABAergic interneurons in the pathogenesis of ASD.

Jun ’07 – May ’09PostDoc research experience on “Malformation of cortical development and epilepsy: genotype-phenotype correlation” at the Neurogenetics Lab, Child Neurology Unit, “A. Meyer” Children’s Hospital, Florence (Head Prof. R. Guerrini). The project aim was to identify new candidate genes for cortical malformations syndromes and to perform genotype-phenotype correlation using in uteroelectroporation and RNAi in rats [in collaboration with Dr. Carlos Cardoso at INSERM/INMED, Marseille].

May ’05 – May ’07PostDoc research experience on “New experimental models for Parkinson’s disease” at the Neuroscience Department, University of Pisa (Head Prof. G.U. Corsini). Aim of the study was to investigate pre-symptomatic compensatory changes occurring in the brain upon chronic long-lasting degeneration. We assessed neurochemical, behavioural and electrophysiogical changes in young and aged EnHTmice. Data suggest that, despite the early degeneration of DA cell bodies, frank behavioral deficits and synaptic plasticity alterations appear only in old mice and that the extracellular metabolism may have a prominent role in the establishment of these compensatory changes. Overall the study suggest the EnHT mouse as a key model of nigrostriatal degeneration and supports its use in the study of neurorestorative therapies for Parkinson’s disease.

Feb ’00 – Dec ’04PhD project: “Development and maintenance of mesencephalic dopaminergic neurons: role of the Engrailedand Pbx1transcription factors”. Aim of the project was to study the role of the Engrailedtranscription factors in the development and maintenance of mesencephalic DA neurons and their interaction with their homeobox Pbx1cofactor. Supervisor: Dr. H.H. Simon, Interdisciplinary Centre for Neuroscience, Department of Neuroanatomy III, University of Heidelberg, Germany.

Apr ’96 – Apr ’99          Master Thesis: “In vivoPC3 overexpression by retroviral vector affects cell differentiation of rat cortical precursors.” The project aimed at investigating the functional role of the anti-proliferative gene PC3(Tis21, Btg2) during development of the cerebral cortex, using in uteroinjection of replication incompetent retroviral vectors. Supervisor: Dr. F. Cremisi, Scuola Normale Superiore, Pisa.

Societies memberships

Member of the Italian Neuroscience Society (SINS)

Member of the Federation of the European Neuroscience Societies (FENS)

Reviewing committees

Peer-review Journals

Neuroscience

Epilepsy Research

Research in Developmental Disabilities

International Journal of Molecular Sciences

Biochemical Science

Archives Italiennes de Biologie

Expert Panel Member

Expert Scientific Review Wellcome Trust

1. Neurobiology of social behaviors – September 2023 – Erice, Italy. “Embryonic exposure to valproic acid alters visual preference for face-like stimuli and mesencephalic dopaminergic distribution and signaling in domestic chicks.”
2. CogEvo 2023 – July 2023 – Rovereto, Italy. “Embryonic exposure to valproic acid alters visual preference for Face-Like stimuli and mesencephalic dopaminergic distribution and signaling in domestic chicks.”
3. Neuroscience Meeting 2022 – November 2022 – San Diego, US. “Fetal blockade of nicotinic acetylcholine transmission causes autism-like impairments of social attachment formation in domestic chicks; recovery by postnatal bumetanide”.
4. 13th FENS Virtual Forum of Neuroscience – July 2022 – Paris, France. “Embryonic exposure to valproic acid impairs visual preferences for Face-Like stimuli and alters dopaminergic distribution and signaling in domestic chicks”.
5. Gordon Research Conference 2002 – Fragile X and Autism-Related Disorders Novel Technologies to Advance Discovery of Disease Mechanisms and Therapeutics for Fragile X and Autism – May 2022 – Lucca, Italy. “Embryonic exposure to valproic acid impairs visual preferences for Face-Like stimuli and alters dopaminergic distribution and signaling in domestic chicks”.
6. 12th FENS Virtual Forum of Neuroscience – July 2020. E-poster title: “Altered social predispositions in chicks exposed to valproate during embryonic development: neurobiological correlates”.
7. 11th FENS Forum of Neuroscience – July 2018 – Berlin, Germany. Poster. “Altered social predispositions in chicks exposed to valproate during embryonic development”.
8. 8th EMCCS-FENS meeting – July 2018 – Berlin, Germany. Poster. “Altered social predispositions in chicks exposed to valproate during embryonic development”.
9. “Wiring the Brain” Cold Spring Harbor Laboratory meeting – April 2017 – Cold Spring Harbor, USA. Invited speaker. “Altered social predispositions in chicks exposed to valproate during embryonic development”.
10. International Meeting for Autism Research – IMFAR 2014 – May 2014, Atlanta, USA. “Transcriptome Profiling in Engrailed2 Knockout Mice Reveals Common Molecular Pathways Associated with Autism Spectrum Disorders”.
11. Neuroscience 2013 – SfN Annual Meeting 2013 – November 2013, San Diego, USA. “Transcriptome profiling in Engrailed2 knockout mice reveals convergent molecular pathology associated with ASD.”
12. “Wiring the Brain” Cold Spring Harbor Laboratory meeting – July 2013, Cold Spring Harbor, USA. “Transcriptome profiling in Engrailed2 knockout mice reveals convergent molecular pathology associated with ASD”
13. Neuroscience 2012 – SfN Annual Meeting 2012 – October 2012, New Orleans, USA. “GABAergic system dysfunction and gene expression profiling alterations in Engrailed2 knockout mice, a model for autism spectrum disorders.”
14. Jacques Monod Conference – “Mechanisms of Intellectual Disability: from genes to treatment”, October 2012, Roscoff, France. “GABAergic system dysfunction and gene expression profiling alterations in Engrailed2 knockout mice, a model for autism spectrum disorders”
15. XIII National Congress of the Italian Society for Neuroscience – October 2009, Milano, Italy. Invited Speaker “Common developmental bases of epilepsy and autism: altered GABAergic innervation in mice lacking the homeobox gene Engrailed 2”.
16. LIMPE Seminars 2009 – February 2009, Pisa, Italy. Invited Speaker “New experimental models of Parkinson’s disease”.
17. LICE 2009 – January 2009, Rome, Italy Invited Speaker “Delezione 6q ed eterotopia periventricolare. Individuazione di geni candidati”
18. LIMPE Seminars 2007 – September 2007, Alghero, Italy. Invited Speaker “Characterization of the Engrailed mutant mice as experimental models for Parkinson's disease”.
19. LIMPE Annual Meeting 2006 - November 2006, Stresa, Italy. Short communication talk: “Perdita Progressiva Dei Neuroni Dopaminergici Della Substantia Nigra In Topi Mutanti Engrailed”. Awarded as best short communication.
20. FENS Meeting 2006 – July 2006, Vienna, Austria. "Characterization of engrailed mutant mice as experimental model for Parkinson¹s Disease: neurochemical and neuropathological features"
21. ICPD 2005 – June 2005, Berlin, Germany. “Progressive postnatal degeneration of nigral dopaminergic neurons in engrailed mutant mice”.
22. FENS Meeting 2004 – July 2004, Lisbon, Portugal. “Progressive postnatal degeneration of nigral dopaminergic neurons in engrailed mutant mice”.
23. The Cell Biology of the Neuron - 33th Neuroscience Meeting, Nov. 2003 – New Orleans, USA. "Progressive loss of nigral dopaminergic neurons in En1+/-,En2-/- adult mice: a mouse model for Parkinson’s Disease".
24. VII National Congress of the Italian Society for Neuroscience – September 2003, Pisa, Italy. Short communication talk. "Progressive postnatal loss of nigral dopaminergic neurons in mutant mice heterozygous null for Engrailed-1 and homozygous null for Engrailed-2". 
25. Gordon Research Conference 2002 – Neural Development – Aug. 2002, Newport, USA. "Role of Pbx1 in the development of the midbrain dopaminergic neurons".
26. FENS Meeting 2002 – July 2002, Paris, France. "Role of Pbx1 in the development of the midbrain dopaminergic neurons".
27. 14th IIGB Meeting – Generating Cell Diversity in the Nervous System – Oct. 2001, Capri, Italy. ”Role of Pbx-1 in the development of midbrain dopaminergic neurons”.