title: Prolactin as a biomarker for treatment response and tardive  dyskinesia in schizophrenia subjects: old thoughts revisited  from a genetic perspective.
abstract: Previous studies investigated whether prolactin (PRL) serum level was a biomarker of antipsychotic response, schizophrenia symptomatology, and tardive dyskinesia. Most of the findings support that antipsychotic drugs modulate PRL levels but PRL is not a steady indicator. Recent results suggest a genetic effect of PRL and PRL receptor (PRLR) polymorphisms in PRL levels indicating that independently of antipsychotic therapy subjects could have altered PRL levels due to their genetic background.We evaluated whether PRL and PRLR variants were associated with treatment outcome and tardive dyskinesia. We observed no association of PRL/PRLR polymorphism with treatment response (best genotypic results include PRL rs849885 and PRLR rs4703509 permuted p=0.326). Regarding tardive dyskinesia, the major allele of PRL rs37364 was nominally associated with risk for tardive dyskinesia in the European ancestry sub-sample (permuted p=0.183). Although we reported no significant associations, it is definitely worthy of investigation to see if together (genetic variants in the PRL system and PRL serum measures) could be a reliable biomarker for antipsychotic response and TD prevalence. Our results suggest that more studies in this context are required to shed light in the molecular mechanisms underlying antipsychotic response and tardive dyskinesia occurrence.
authors.affiliation: Neurogenetics Section, Neuroscience Department, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. renanrps@yahoo.com.br
authors.forename: Renan P
authors.initials: RP
authors.lastname: Souza
authors.forename: Herbert Y
authors.initials: HY
authors.lastname: Meltzer
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Lieberman
authors.forename: Aristotle N
authors.initials: AN
authors.lastname: Voineskos
authors.forename: Gary
authors.initials: G
authors.lastname: Remington
authors.forename: James L
authors.initials: JL
authors.lastname: Kennedy
mesh_terms: D000328:Adult; D000483:Alleles; D014150:Antipsychotic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D015415:Biomarkers / Q000378:metabolism; D003024:Clozapine / Q000009:adverse effects / Q000627:therapeutic use; D004409:Dyskinesia, Drug-Induced / Q000209:etiology*; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011388:Prolactin / Q000097:blood*; D011446:Prospective Studies; D011981:Receptors, Prolactin / Q000235:genetics*; D012559:Schizophrenia / Q000188:drug therapy*; D016896:Treatment Outcome; D044465:White People; D055815:Young Adult
chemical_list: D014150:Antipsychotic Agents; D015415:Biomarkers; D011981:Receptors, Prolactin; D011388:Prolactin; D003024:Clozapine