No abstract

Cell 159, 33-45; September 25, 2014) During the preparation of Figure 1 in the article above, we inadvertently included lines separating the lanes in the western blot shown in Figure 1E. In that panel, the Vinculin control for ARC should not display separating lines, as all samples were loaded on consecutive lanes. We would like to clarify that the legends of Figures 1 and 2 should have indicated that the separating lines demarcate bands that come from nonconsecutive lanes of the same gel. Finally, in the legend of Figure 1, we did not mention that the Vinculin loading control for ARC and CamKIIa shown in Figure 1E is the same, as these proteins were detected in the same membrane. The errors do not in any way affect the results or interpretation of the figure. We apologize for any confusion that these errors may have caused.

No abstract

Elevated cerebrospinal fluid (CSF) levels of the glia-derived N-methyl-d-aspartic acid receptor antagonist kynurenic acid (KYNA) have consistently been implicated in schizophrenia and bipolar disorder. Here, we conducted a genome-wide association study based on CSF KYNA in bipolar disorder and found support for an association with a common variant within 1p21.3. After replication in an independent cohort, we linked this genetic variant—associated with reduced SNX7 expression—to positive psychotic symptoms and executive function deficits in bipolar disorder. A series of post-mortem brain tissue and in vitro experiments suggested SNX7 downregulation to result in a caspase-8-driven activation of interleukin-1β and a subsequent induction of the brain kynurenine pathway. The current study demonstrates the potential of using biomarkers in genetic studies of psychiatric disorders, and may help to identify novel drug targets in bipolar disorder.