Identification of a naturally occurring 21 bp deletion in alpha2c noradrenergic receptor gene and cognitive correlates to antipsychotic treatment

Vincenzo De Luca, John B. Vincent, Daniel J. Müller, Rudi Hwang, Takahiro Shinkai, Jan Volavka, Pal Czobor, Brian B. Sheitman, Jean Pierre Lindenmayer, Leslie Citrome, Joseph Patrick McEvoy, Jeffrey A. Lieberman, James L. Kennedy

Research output: Contribution to journalArticle

6 Scopus citations


Neurocognitive deficits are recognized as a cardinal feature of schizophrenia. Atypical antipsychotics have high affinity for many neurotransmitter receptors. Among these receptors, antipsychotics are antagonists of adrenoceptors, and this pharmacological property has been postulated to be involved in the mechanism of action of antipsychotics. We tested the hypotheses that clinical response and cognitive improvement to antipsychotic treatment are associated with genetic variation in adrenergic α2C receptor (ADRA2C). Fifty-seven patients with chronic schizophrenia were prospectively assessed for clinical response to antipsychotic treatment. They were subsequently genotyped for a 21 bp insertion/deletion that we identified in the 3′ untranslated region (3′UTR) of ADRA2C. With regard to clinical response and cognitive improvement to antipsychotics, there was no significant association observed for this polymorphism. Our results suggest that the novel polymorphism may not play a major role in antipsychotic response.

Original languageEnglish (US)
Pages (from-to)381-384
Number of pages4
JournalPharmacological Research
Issue number4
Publication statusPublished - Apr 2005
Externally publishedYes



  • Adrenergic α receptor (ADRA2C)
  • Antipsychotic response
  • Cognition
  • Polymorphism
  • Schizophrenia

ASJC Scopus subject areas

  • Pharmacology

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