Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9015265 | Pharmacological Research | 2005 | 4 Pages |
Abstract
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 3â² untranslated region (3â²UTR) 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.
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Authors
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 P. McEvoy, Jeffrey A. Lieberman, James L. Kennedy,