DHEA treatment improved memory recollection and mood and decreased trough cortisol levels. The effect of DHEA appears to be via neuronal recruitment of the steroid sensitive ACC that may be involved in pre-hippocampal memory processing. These findings are distinctive, being the first to show such beneficial effects of DHEA on memory in healthy young men.

A major issue in proof of concept studies and early clinical trials of novel therapeutic agents is that the active drugs can often have a relatively small additional effect compared with placebo. This is especially the case in psychiatry when we usually have no direct method of measuring the pathology underlying the disorder being studied but, rather, have to rely on the subjective assessment of psychiatric symptoms. The use of the electroencephalogram (EEG) offers two potential major means of addressing this problem. First it is able to provide direct data relating to neural activity that may be abnormal in certain disorders. As such there are opportunities for utilizing the EEG in a variety of ways as an objective outcome measure. Second there is growing evidence that in certain circumstances the EEG can be used to predict which patients are likely to respond to treatment, thus potentially increasing the power of studies by decreasing non-response rates and increasing mean changes in outcome measure. Both of these uses of the EEG are illustrated in reference to the study of mood disorders and in particular depression and its treatment with antidepressants.

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We report a consanguineous family in which schizophrenia segregates in a manner consistent with recessive inheritance of a rare, partial-penetrance susceptibility allele. From 4 marriages between 2 sets of siblings who are half first cousins, 6 offspring have diagnoses of psychotic disorder. Homozygosity mapping revealed a 6.1-Mb homozygous region on chromosome 13q22.2-31.1 shared by all affected individuals, containing 13 protein-coding genes. Microsatellite analysis confirmed homozygosity for the affected haplotype in 12 further apparently unaffected members of the family. Psychiatric reports suggested an endophenotype of milder psychiatric illness in 4 of these individuals. Exome and genome sequencing revealed no potentially pathogenic coding or structural variants within the risk haplotype. Filtering for noncoding variants with a minor allele frequency of <0.05 identified 17 variants predicted to have significant effects, the 2 most significant being within or adjacent to the SCEL gene. RNA sequencing of blood from an affected homozygote showed the upregulation of transcription from NDFIP2 and SCEL. NDFIP2 is highly expressed in brain, unlike SCEL, and is involved in determining T helper (Th) cell type 1 and Th2 phenotypes, which have previously been implicated with schizophrenia.