AD/HD shows a high comorbidity among obese hospitalized children. The characteristic difficulty in regulation found in AD/HD may be a risk factor for the development of abnormal eating behaviors leading to obesity. We suggest that obese children should be screened routinely for AD/HD.

In sorrow thou shalt bring forth children (Genesis 3:16) seems as relevant today, with one of seven mothers afflicted by a depressive episode, constituting the most common medical complication after delivery. Why mothers are variably affected by mood symptoms postpartum remains unclear, and the pathogenesis and early molecular indicators of this divergent outcome have not been described. We applied a case-control design comparing differential global gene expression profiles in blood mononuclear cells sampled shortly after delivery at the time of inception of postpartum depression (PD). Nine antidepressant naive mothers showing high depressive scores and developing a persisting major depressive episode with postpartum onset were compared with 10 mothers showing low depressive scores and no depressive symptoms on prospective follow-up. A distinctive gene expression signature was observed after delivery among mothers with an emergent PD, with a significant overabundance of transcripts showing a high-fold differential expression between groups, and correlating with depressive symptom severity among all mothers. Early expression signatures correctly classified the majority of PD patients and controls. Those developing persisting PD exhibit a relative downregulation of transcription after delivery, with differential immune activation, and decreased transcriptional engagement in cell proliferation, and DNA replication and repair processes. Our data provide initial evidence indicating that blood cells sampled shortly after delivery may harbor valuable prognostic information for identifying the onset of persisting PD. Some of the informative transcripts and pathways may be implicated in the differential vulnerability that underlies depression pathogenesis.

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Anderson-Fabry disease (AFD) is an X-linked inherited lysosomal storage disorder disease caused by a deficiency in the activity of the alpha-galactosidase enzyme. We investigated neuropsychological and psychiatric function in AFD patients. We studied 16 AFD patients, aged 7 to 61 years. Intelligence, language, vision-spatial abilities, memory, sensorimotor abilities, and attention and executive functions were tested with a computerized test battery as well as standard paper and pencil tests. The results were compared to known age-based norms. In addition, all patients were screened for lifelong DSM-IV Axis-I and Axis-II psychiatric diagnoses, and 4 were interviewed by a psychiatrist. Performance on most cognitive measures was within average range. All measures of information processing speed were significantly reduced, as were some measures of executive functions. Ten out of 16 patients met DSM-IV criteria for Axis I or Axis II diagnoses at some point in their lives. This preliminary study delineates a psychiatric and cognitive phenotype in AFD patients and contributes to the growing field of characterizing behavioral phenotypes of patients with genetic diseases. We suggest that psychiatric and neuro-psychological evaluation be included in the patient's evaluation.

Keywords: attention deficit hyperactivity disorder; ADHD; interleukin-1 receptor antagonist gene; transmission disequilibrium test