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Striatal and Extrastriatal Dopamine Transporter Availability in Schizophrenia and Its Clinical Correlates: A Voxel-Based and High-Resolution PET Study.

Artiges E, Leroy C, Dubol M, Prat M, Pepin A, Mabondo A, de Beaurepaire R, Beaufils B, Korwin J-P, Galinowski A, et al.
Schizophr Bull. 2017 Feb 08. PMID: 28177089. Pubmed

Comments

Submitted by Anissa Abi-Dargham on

The study by Artiges and colleagues is intriguing: It contradicts many other studies that do not find an increase in DAT in schizophrenia, as described by the authors. In order to better evaluate the data included in the paper, I would have liked to see the values of the outcome measures rather than only the results of the SPM analysis. What were the BPNDs in the different regions? How different were the values across the groups, and the regional variations? Without such information, it is difficult to comment on the paper.

The finding of increased DAT is not consistent with our own finding of reduced release of dopamine in extrastriatal regions (Slifstein et al., 2015). Since we measured amphetamine-induced dopamine release, we would expect an increase in DAT to potentiate the amphetamine effect. However, there could be more complex, and speculatory, explanations that could attempt to reconcile these findings. The perspective of the authors on this inconsistency would have been helpful.

Finally, it is worth noting some technical limitations: In particular, the use of a reference region as a “proxy” for the input function has the potential of contributing to the group differences; furthermore, Artiges and colleagues do not appear to have scanned long enough for the striatum to yield a robust and reliable outcome measure (60 minutes instead of 70 or 80).

Nevertheless, the story outside of the striatum is getting more interesting. Replications are needed for both sets of findings―the DAT increase and the DA release deficit.