Describing for the first time a COP2 transport defect that causes psychosis - go to preview function for free access.

In a familial disorder that can cause psychosis that is comorbid with physical symptoms of various metabolic disorders, evidence is presented which indicates that the metabolic derangement in the disorder likely centers on the hypofunction of SAR1B mediated COP2 transport, and the consequential hyperfunction of SAR1B/COP2 autophagy. This metabolic derangement has significant links to five genetic locations, three of which were previously reported on in the disorder – 5q31.1, 17p11.2 and 17p13.1. It is noted that a complete or partial failure of the PI3K product PI3P, or of PI4KA dependent PI4P, to bind with SEC23IP, as part of the COP2 transport process, would be almost entirely consistent with and provide a complete explanation for the presentation of this familial disorder.