Andrea De Bartolomeis
e-mail: adebarto AT unina.it
website: www.unina.it
affiliation: Università di Napoli Federico II
research area(s): Neuroscience
Course:
Neurosciences
University/Istitution: Università di Napoli Federico II
University/Istitution: Università di Napoli Federico II
Andrea de Bartolomeis M.D. Ph.D, received his medical degree and his residency training in psychiatry at the University Federico II of Naples, Italy. He completed his postdoctoral fellowship in psychopharmacology and molecular pathophysiology of schizophrenia with NIMH in Bethesda MD (USA) at Clinical Neuroscience Branch (1989-1992) and at Experimental Therapeutics Branch (1993-1994) where he contributed to develop a novel method for quantitation of synaptic dopamine in vivo in primates, using PET and microdialysis simultaneously.
In 1998 he received from the University of Naples a Ph.D. degree in Methodology of Communication Science.
Dr. de Bartolomeis is currently Associate Professor of Psychiatry at Department of Neuroscience and Behavioral Sciences and Professor of Molecular Psychiatry and Psychopharmacology in the Residency Program of Clinical Psychiatry of the University Federico II of Naples.
He is Chief of the Laboratory of Molecular Psychiatry and he is in charge of the Outpatient Clinics for Treatment Resistant Psychosis. The research interest of Andrea de Bartolomeis include the molecular pathophysiology of psychosis, CNS gene expression modulation by psychotropic drugs, and augmentation strategy in psychosis pharmacotherapy.
He has been principal investigator or co-investigator on several research and training grants as well on clinical trials from public and drug company sources.
He has authored many papers, book chapters and published abstracts on molecular mechanisms of antipsychotics as well as on schizophrenia pathophysiology and molecular imaging of dopaminergic system. He published his works in leading journals including Nature in Medicine, Proceedings of national Academy of Sciences, Biological Psychiatry, Neuropsychopharmacology, MoleculaR Brain Research, Synapse, Cerebral Blood FLOW and Metabolism .
His recent research is focusing on antipsychotics impact on postsynaptic density scaffolding proteins and molecular mechanisms of antipsychotics augmentation by glicine partial agonists.
In 1998 he received from the University of Naples a Ph.D. degree in Methodology of Communication Science.
Dr. de Bartolomeis is currently Associate Professor of Psychiatry at Department of Neuroscience and Behavioral Sciences and Professor of Molecular Psychiatry and Psychopharmacology in the Residency Program of Clinical Psychiatry of the University Federico II of Naples.
He is Chief of the Laboratory of Molecular Psychiatry and he is in charge of the Outpatient Clinics for Treatment Resistant Psychosis. The research interest of Andrea de Bartolomeis include the molecular pathophysiology of psychosis, CNS gene expression modulation by psychotropic drugs, and augmentation strategy in psychosis pharmacotherapy.
He has been principal investigator or co-investigator on several research and training grants as well on clinical trials from public and drug company sources.
He has authored many papers, book chapters and published abstracts on molecular mechanisms of antipsychotics as well as on schizophrenia pathophysiology and molecular imaging of dopaminergic system. He published his works in leading journals including Nature in Medicine, Proceedings of national Academy of Sciences, Biological Psychiatry, Neuropsychopharmacology, MoleculaR Brain Research, Synapse, Cerebral Blood FLOW and Metabolism .
His recent research is focusing on antipsychotics impact on postsynaptic density scaffolding proteins and molecular mechanisms of antipsychotics augmentation by glicine partial agonists.
The glutamergic postsynaptic density is a specializzation of synapse that che be distinguished as electro-dense thickness under electron microscopy. Hundreds of proteins with scaffolding, trafficking and signal "trasduction function have been described at glutamatergic postsynaptic density .Homer is a family of PSD proteins : both constitutive (Homer 1 b/c, Homer 2, Homer 3)and inducile (Homer 1a) forms have been reported. Several lines of evidence suggest a relevant role of Homer in cortical and sub-cortical dopamine-glutamate interaction (de Bartolomeis et al., 2005). Homer has been demonstrated to be involved in cell surface clustering of Tipe I metabotropic receptors, as well as in neural palsticity induced by behavioral, electrophysiological and pharmacological stimuli (Bottai et al., 2002). Recently, a potential involvement of Homer in neuropsychiatric diseases has been suggested.
Aims of the present research lone are to investigate:
1. putative epigenetic modulation of PSD genes after prolonged NMDA receptor antagonism by ketamine in animal model of NMDA hypofunction relevant to schizophrenia pathophysiology
2. the differential induction of Homer1a by structurally different NMDA antagonist (Ketamine, MK 801, Memantine) .
3. the role of postsynaptic density proteins in the animal pharmacological isomorphisms of antipsychotics augmentation by glycine transporter inhibitors.
Homer gene expression will be investigated with molecular imaging tecnique, mainly in situ hybridization histochemistry. The products of transcription will be analyzed also by RT-PCR.
Western-blot and immunohistochemistry will be performed to characterize PSD changes at translational level. A in silico approach is also considered in order to identify the candidate network gene that may crosstalk with Homer signaling and be affected as well by antipsychotic drugs.
Aims of the present research lone are to investigate:
1. putative epigenetic modulation of PSD genes after prolonged NMDA receptor antagonism by ketamine in animal model of NMDA hypofunction relevant to schizophrenia pathophysiology
2. the differential induction of Homer1a by structurally different NMDA antagonist (Ketamine, MK 801, Memantine) .
3. the role of postsynaptic density proteins in the animal pharmacological isomorphisms of antipsychotics augmentation by glycine transporter inhibitors.
Homer gene expression will be investigated with molecular imaging tecnique, mainly in situ hybridization histochemistry. The products of transcription will be analyzed also by RT-PCR.
Western-blot and immunohistochemistry will be performed to characterize PSD changes at translational level. A in silico approach is also considered in order to identify the candidate network gene that may crosstalk with Homer signaling and be affected as well by antipsychotic drugs.
Panariello F, Perruolo G, Cassese A, Giacco F, Botta G, Barbagallo AP, Muscettola G, Beguinot F, Formisano P, de Bartolomeis A. (2011) Clozapine impairs insulin action by up-regulating Akt phosphorylation and Ped/Pea-15 protein abundance. J Cell Physiol. 2011 May 26
TOMASETTI C, DELL'AVERSANO C, IASEVOLI F, MARMO F, DE BARTOLOMEIS A. (2011). The acute and chronic effects of combined antipsychotic-mood stabilizing treatment on the expression of cortical and striatal postsynaptic density genes. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY. pp. 14:184-197
IASEVOLI F, TOMASETTI C, MARMO F, BRAVI D, ARNT J, DE BARTOLOMEIS A (2010). Divergent acute and chronic modulation of glutamatergic postsynaptic density genes expression by the antipsychotics haloperidol and sertindole. . PSYCHOPHARMACOLOGY. pp. 16:329-344
IASEVOLI F, FIORE G, CICALE M, MUSCETTOLA G, DE BARTOLOMEIS A. (2010). Haloperidol induces higher Homer1a expression than risperidone, olanzapine and sulpiride in striatal sub-regions. PSYCHIATRY RESEARCH. pp. 6:255-260
IASEVOLI F, TOMASETTI C, AMBESI-IMPIOMBATO A, MUSCETTOLA G, DE BARTOLOMEIS A (2009). Dopamine receptor subtypes contribution to Homer1a induction: Insights into antipsychotic molecular action. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY. pp. 9:813-821
DELL'AVERSANO C, TOMASETTI C, IASEVOLI F, DE BARTOLOMEIS A (2009). Antipsychotic and antidepressant co-treatment: effects on transcripts of inducible postsynaptic density genes possibly implicated in behavioural disorders. BRAIN RESEARCH BULLETIN. pp. 7:123-129
DE LUCA V, ANNESI G, DE MARCO EV, DE BARTOLOMEIS A, NICOLETTI G, PUGLIESE P, MUSCETTOLA G, BARONE P, QUATTRONE A (2009). HOMER1 promoter analysis in parkinson's disease: association study with psychotic symptoms. NEUROPSYCHOBIOLOGY. pp. 7:239-245
PALUMBO P, ERAMO A, DE BARTOLOMEIS A (2008). Janus's face of schizophrenia treatment: neurobiology of antipsychotic treatments response and resistance . RIVISTA DI PSICHIATRIA. pp. 23:269-291
SOUZA RP, DE LUCA V, MUSCETTOLA G, ROSA DV, DE BARTOLOMEIS A, ROMANO SILVA M, KENNEDY JL (2008). Association of antipsychotic induced weight gain and body mass index with GNB3 gene: A meta-analysis. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY. pp. 6:1848-1853
IASEVOLI F, POLESE D, AMBESI-IMPIOMBATO A, MUSCETTOLA G, DE BARTOLOMEIS A (2007). Ketamine-related expression of glutamatergic postsynaptic density genes: possible implications in psychosis. NEUROSCIENCE LETTERS. pp. 5:1-5
TOMASETTI C, DELL'AVERSANO C, IASEVOLI F, DE BARTOLOMEIS A (2007). Homer splice variants modulation within cortico-subcortical regions by dopamine D2 antagonists, a partial agonist, and an indirect agonist: implication for glutamatergic postsynaptic density in antipsychotics action. NEUROSCIENCE. pp. 15:144-158
TOMASETTI C, DELL'AVERSANO C, IASEVOLI F, MARMO F, DE BARTOLOMEIS A. (2011). The acute and chronic effects of combined antipsychotic-mood stabilizing treatment on the expression of cortical and striatal postsynaptic density genes. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY. pp. 14:184-197
IASEVOLI F, TOMASETTI C, MARMO F, BRAVI D, ARNT J, DE BARTOLOMEIS A (2010). Divergent acute and chronic modulation of glutamatergic postsynaptic density genes expression by the antipsychotics haloperidol and sertindole. . PSYCHOPHARMACOLOGY. pp. 16:329-344
IASEVOLI F, FIORE G, CICALE M, MUSCETTOLA G, DE BARTOLOMEIS A. (2010). Haloperidol induces higher Homer1a expression than risperidone, olanzapine and sulpiride in striatal sub-regions. PSYCHIATRY RESEARCH. pp. 6:255-260
IASEVOLI F, TOMASETTI C, AMBESI-IMPIOMBATO A, MUSCETTOLA G, DE BARTOLOMEIS A (2009). Dopamine receptor subtypes contribution to Homer1a induction: Insights into antipsychotic molecular action. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY. pp. 9:813-821
DELL'AVERSANO C, TOMASETTI C, IASEVOLI F, DE BARTOLOMEIS A (2009). Antipsychotic and antidepressant co-treatment: effects on transcripts of inducible postsynaptic density genes possibly implicated in behavioural disorders. BRAIN RESEARCH BULLETIN. pp. 7:123-129
DE LUCA V, ANNESI G, DE MARCO EV, DE BARTOLOMEIS A, NICOLETTI G, PUGLIESE P, MUSCETTOLA G, BARONE P, QUATTRONE A (2009). HOMER1 promoter analysis in parkinson's disease: association study with psychotic symptoms. NEUROPSYCHOBIOLOGY. pp. 7:239-245
PALUMBO P, ERAMO A, DE BARTOLOMEIS A (2008). Janus's face of schizophrenia treatment: neurobiology of antipsychotic treatments response and resistance . RIVISTA DI PSICHIATRIA. pp. 23:269-291
SOUZA RP, DE LUCA V, MUSCETTOLA G, ROSA DV, DE BARTOLOMEIS A, ROMANO SILVA M, KENNEDY JL (2008). Association of antipsychotic induced weight gain and body mass index with GNB3 gene: A meta-analysis. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY. pp. 6:1848-1853
IASEVOLI F, POLESE D, AMBESI-IMPIOMBATO A, MUSCETTOLA G, DE BARTOLOMEIS A (2007). Ketamine-related expression of glutamatergic postsynaptic density genes: possible implications in psychosis. NEUROSCIENCE LETTERS. pp. 5:1-5
TOMASETTI C, DELL'AVERSANO C, IASEVOLI F, DE BARTOLOMEIS A (2007). Homer splice variants modulation within cortico-subcortical regions by dopamine D2 antagonists, a partial agonist, and an indirect agonist: implication for glutamatergic postsynaptic density in antipsychotics action. NEUROSCIENCE. pp. 15:144-158
Project Title:
Cortical and subcortical dopamine-glutamate interaction and PSD proteins involvement:focus on Homer and related proteins. Implications for behavioral
The glutamergic postsynaptic density is a specializzation of synapse that che be distinguished as electro-dense thickness under electron microscopy. Hundreds of proteins with scaffolding, trafficking and signal �trasduction function have been described at glutamatergic postsynaptic density .Homer is a family of PSD proteins : both constitutive (Homer 1 b/c, Homer 2, Homer 3)and inducile (Homer 1a) forms have been reported.
Several lines of evidence suggest a relevant role of Homer in cortical and sub-cortical dopamine-glutamate interaction (de Bartolomeis et al., 2005).
Homer has been demonstrated to be involved in cell surface clustering of Tipe I metabotropic receptors, as well as in neural palsticity induced by behavioral, electrophysiological and pharmacological stimuli (Bottai et al., 2002). Recently, a potential involvement of Homer in neuropsychiatric diseases has been suggested.
Aims of the study
1. To investigate putative epigenetic modulation of PSD genes after prolonged NMDA receptor antagonism by ketamine in animal model of NMDA hypofunction relevant to schizophrenia pathophysiology
2. To investigate the differential induction of Homer1a by structurally different NMDA antagonist (Ketamine, MK 801, Memantine) .
3. To investigate the role of postsynaptic density proteins in the animal pharmacological isomorphisms of antipsychotics augmentation by glycine transporter inhibitors.
Methodology
Homer gene expression will be investigated with molecular imaging tecnique, mainly in situ hybridization histochemistry. The products of transcription will be analyzed also by RT-PCR.
Western-blot and immunohistochemistry will be performed to characterize PSD changes at translational level.
A in silico approach is also considered in order to identify the candidate network gene that may crosstalk with Homer signaling and be affected as well by antipsychotic drugs.
Several lines of evidence suggest a relevant role of Homer in cortical and sub-cortical dopamine-glutamate interaction (de Bartolomeis et al., 2005).
Homer has been demonstrated to be involved in cell surface clustering of Tipe I metabotropic receptors, as well as in neural palsticity induced by behavioral, electrophysiological and pharmacological stimuli (Bottai et al., 2002). Recently, a potential involvement of Homer in neuropsychiatric diseases has been suggested.
Aims of the study
1. To investigate putative epigenetic modulation of PSD genes after prolonged NMDA receptor antagonism by ketamine in animal model of NMDA hypofunction relevant to schizophrenia pathophysiology
2. To investigate the differential induction of Homer1a by structurally different NMDA antagonist (Ketamine, MK 801, Memantine) .
3. To investigate the role of postsynaptic density proteins in the animal pharmacological isomorphisms of antipsychotics augmentation by glycine transporter inhibitors.
Methodology
Homer gene expression will be investigated with molecular imaging tecnique, mainly in situ hybridization histochemistry. The products of transcription will be analyzed also by RT-PCR.
Western-blot and immunohistochemistry will be performed to characterize PSD changes at translational level.
A in silico approach is also considered in order to identify the candidate network gene that may crosstalk with Homer signaling and be affected as well by antipsychotic drugs.