A1 Refereed original research article in a scientific journal
Striatal dopamine transporter binding in neuroleptic-naive patients with schizophrenia studied with positron emission tomography
Authors: Laakso A, Vilkman H, Alakare B, Haaparanta M, Bergman J, Solin O, Peurasaari J, Rakkolainen V, Syvalahti E, Hietala J
Publisher: AMER PSYCHIATRIC PRESS, INC
Publication year: 2000
Journal: American Journal of Psychiatry
Journal name in source: AMERICAN JOURNAL OF PSYCHIATRY
Journal acronym: AM J PSYCHIAT
Volume: 157
Issue: 2
First page : 269
Last page: 271
Number of pages: 3
ISSN: 0002-953X
DOI: https://doi.org/10.1176/appi.ajp.157.2.269
Abstract
Objective: Recent in vivo imaging studies indicate a dysregulated presynaptic function of the striatal dopaminergic system in patients with schizophrenia. To further explore the basis of this phenomenon, the authors studied brain dopamine transporter binding in vivo in patients with first-episode, never-medicated schizophrenia. Method: Nine patients with schizophrenia and nine healthy matched comparison subjects were recruited. Striatal dopamine transporter binding was measured with positron emission tomography and a specific dopamine transporter ligand, [F-18]CFT, a radiolabeled form of 2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane. Results: Average caudate and putamen dopamine transporter binding potentials were almost identical in the patients and comparison subjects, but the patients lacked the right-left asymmetry of the caudate dopamine transporter binding seen in the comparison group. Conclusions: Average striatal dopamine transporter density is unaltered in neuroleptic-naive patients with schizophrenia. However, patients lack asymmetry in caudate dopamine transporter binding, which conforms with disrupted brain lateralization in this disorder.
Objective: Recent in vivo imaging studies indicate a dysregulated presynaptic function of the striatal dopaminergic system in patients with schizophrenia. To further explore the basis of this phenomenon, the authors studied brain dopamine transporter binding in vivo in patients with first-episode, never-medicated schizophrenia. Method: Nine patients with schizophrenia and nine healthy matched comparison subjects were recruited. Striatal dopamine transporter binding was measured with positron emission tomography and a specific dopamine transporter ligand, [F-18]CFT, a radiolabeled form of 2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane. Results: Average caudate and putamen dopamine transporter binding potentials were almost identical in the patients and comparison subjects, but the patients lacked the right-left asymmetry of the caudate dopamine transporter binding seen in the comparison group. Conclusions: Average striatal dopamine transporter density is unaltered in neuroleptic-naive patients with schizophrenia. However, patients lack asymmetry in caudate dopamine transporter binding, which conforms with disrupted brain lateralization in this disorder.
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