title: Postnatal neurogenesis and dopamine alterations in early psychosis.
abstract: Schizophrenia is most likely a neurodevelopmental disorder with a characteristic delayed onset of symptoms occurring usually during transition from adolescence to adulthood. Recent studies revealed that both genetic and environmental risk factors for the disease disturb not only embryonic, but also postnatal neurogenesis, possible contributing to neurochemical alterations associated with schizophrenia. Several recent patents proposed therapeutic interventions in schizophrenia by increasing postnatal neurogenesis. It remains, however, unclear, how such pro-neurogenic interventions could ameliorate alterations in neurotransmitter systems associated with the disease, such as the dopamine system. Here we review these patents in the context of the existent data about postnatal neurogenesis in the subventricular zone in rodents and primates. We discuss also in light of a recently proposed theoretical model the possible relevance of disturbed neurogenesis for the dopamine system, focusing on the dopamine receptors associated with neurogenesis, the D3 receptors, and a D3-expressing structure derived from the subventricular zone, the Islands of Calleja. Finally, we discuss these findings in the light of molecular imaging studies in early schizophrenia.
authors.affiliation: Department of Psychiatry and Psychotherapy, Central Institute for Mental Health Mannheim, University of Heidelberg, J 5, 68159 Mannheim, Germany. Dragos.Inta@zi-mannheim.de
authors.forename: Dragos
authors.initials: D
authors.lastname: Inta
authors.forename: Juan M
authors.initials: JM
authors.lastname: Lima-Ojeda
authors.forename: Peter
authors.initials: P
authors.lastname: Gass
authors.forename: Paolo
authors.initials: P
authors.lastname: Fusar-Poli
mesh_terms: D000293:Adolescent; D041923:Adolescent Development / Q000187:drug effects; D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology / Q000627:therapeutic use; D001479:Basal Ganglia / Q000187:drug effects / Q000378:metabolism*; D002648:Child; D002657:Child Development / Q000187:drug effects; D004298:Dopamine / Q000378:metabolism*; D018492:Dopamine Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D015507:Drugs, Investigational / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D020670:Islands of Calleja / Q000187:drug effects / Q000378:metabolism*; D058990:Molecular Targeted Therapy; D009419:Nerve Tissue Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D055495:Neurogenesis / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010330:Patents as Topic; D011618:Psychotic Disorders / Q000188:drug therapy / Q000378:metabolism*; D050637:Receptors, Dopamine D3 / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D014150:Antipsychotic Agents; C493593:DRD3 protein, human; D018492:Dopamine Antagonists; D015507:Drugs, Investigational; D009419:Nerve Tissue Proteins; D050637:Receptors, Dopamine D3; D004298:Dopamine