Interest has grown in genetic testing to personalize treatment approaches in psychiatry, especially mood disorders and to a lesser extent anxiety. However, numerous studies of genetic variants of metabolizing enzymes, along with fewer studies of single nucleotide polymorphisms of drug transporter proteins, receptors, and other putative drug targets such as neurotransmitter reuptake pumps and receptors, have reported contradictory findings that have not translated into practical, cost-effective treatment recommendations. In this article, we review basic principles of genetic testing and highlight selected elements of genetic testing in cancer. We then critically review the current status of genetic research in pharmacokinetics and pharmacodynamics, as well as the few clinical trials that have been performed. After discussing the limited clinical applications of current research, we make recommendations for developing more clinically useful studies of cost-effective approaches to genetic testing in the treatment of mood and anxiety disorders.

Cognitive impairments are well-documented features of mood and anxiety disorders. Recent developments in research on cognition, assessment techniques, treatments, and comorbidities in cognitive changes across major depression, bipolar disorder, and post-traumatic stress disorder (PTSD) are reviewed. Promising treatments have been reported but are tempered by self-reported cognitive performance and its minimal relationship to objective data. The need for objective assessment as well as assessment of subjective impressions of cognition is discussed. The use of assessment of performance-based measures of everyday functional skills in major depression, bipolar disorder, and PTSD is another critical development highlighted in the present review. The recent success of pharmacological treatments for cognitive impairments in major depressive disorder (MDD) is promising, yet the need for clinicians to assess and consider bias in their treatment outcome data is essential.

Autism is a complex disease with many genetic factors contributing to the variable phenotype presentation. Genome-wide association studies (GWAS) using large cohorts and dense datasets have revealed a myriad of genes implicated in autism. Several of these genes belong to common biological pathways and gene networks that converge on potential therapeutic targets. In this regard, CACNA, GRM, CNTN, ubiquitin, and SLIT gene families have shown promising variants in association with autism and related neurodevelopmental disorders. Both common and rare variants reside on these genes discovered primarily by single nucleotide polymorphism (SNP) arrays and whole exome sequencing. The ability to examine large cohorts through unbiased screening and statistical testing of allele frequencies between cases, families, and controls through GWAS will continue to elucidate and clarify the puzzle of autism and inform clinical care.

Working memory, a theoretical construct from the field of cognitive psychology, is crucial to everyday life. It refers to the ability to temporarily store and manipulate task-relevant information. The identification of genes for working memory might shed light on the molecular mechanisms of this important cognitive ability and-given the genetic overlap between, for example, schizophrenia risk and working-memory ability-might also reveal important candidate genes for psychiatric illness. A number of genome-wide searches for genes that influence working memory have been conducted in recent years. Interestingly, the results of those searches converge on the mediating role of neuronal excitability in working-memory performance, such that the role of each gene highlighted by genome-wide methods plays a part in ion channel formation and/or dopaminergic signaling in the brain, with either direct or indirect influence on dopamine levels in the prefrontal cortex. This result dovetails with animal models of working memory that highlight the role of dynamic network connectivity, as mediated by dopaminergic signaling, in the dorsolateral prefrontal cortex. Future work, which aims to characterize functional variants influencing working-memory ability, might choose to focus on those genes highlighted in the present review and also those networks in which the genes fall. Confirming gene associations and highlighting functional characterization of those associations might have implications for the understanding of normal variation in working-memory ability and also for the development of drugs for mental illness.

Genome wide association studies (GWAS) have revolutionized the study of complex diseases and have uncovered common genetic variants associated with an increased risk for major psychiatric disorders. A recently published schizophrenia GWAS replicated earlier findings implicating common variants in Transcription factor 4 (TCF4) as susceptibility loci for schizophrenia. By contrast, loss of function TCF4 mutations, although rare, cause Pitt-Hopkins syndrome (PTHS); a disorder characterized by intellectual disability (ID), developmental delay and behavioral abnormalities. TCF4 mutations have also been described in individuals with ID and non-syndromic neurodevelopmental disorders. TCF4 is a member of the basic helix-loop-helix (bHLH) family of transcription factors that regulate gene expression at E-box-containing promoters and enhancers. Accordingly, TCF4 has an important role during brain development and can interact with a wide array of transcriptional regulators including some proneural factors. TCF4 may, therefore, participate in the transcriptional networks that regulate the maintenance and differentiation of distinct cell types during brain development. Here, we review the role of TCF4 variants in the context of several distinct brain disorders associated with impaired cognition.

The widespread availability of high speed, mobile cellular telephones and other advances in communication technology have the potential to change the way that interventions for substance use disorders (SUD) are delivered and how progress is monitored. This article reviews recent research on the use of new technology to monitor progress and deliver interventions for SUD. Several studies of telephone-based interventions show positive effects, but sometimes only in certain subgroups. However, other studies produced negative results. Studies support the use of interactive voice response (IVR) and personal digital assistants (PDAs) to conduct assessments, but there is little data on whether IVR- or PDA-based interventions improve outcomes. Text messaging has received comparatively little research, but appears promising as a means to conduct assessments and deliver automated interventions. Finally, smartphone technology provides the widest range of features and interventions and the greatest flexibility, but few intervention studies that use them have been conducted.

Schizophrenia (SCZ) is a severe psychiatric disorder, which lacks a unifying neuropathology. However, reproducible molecular alterations exist, including RNA expression changes affecting GABAergic and other neuronal signaling in cerebral cortex, myelination, and other cellular functions. Yet, for the large majority of RNAs altered in the SCZ brain, the underlying transcriptional and post-transcriptional disease-associated mechanisms remain unclear. Here, we provide an update on epigenetic regulators of gene expression that are potentially affected in some cases with SCZ, including DNA cytosine methylation, histone modifications and histone variants, and chromosomal loop formations facilitating long-range interactions of gene promoters with distal enhancer elements. Exploration of chromatin structure and function, in combination with transcriptome and genome sequencing, is likely to critically advance insight into the molecular mechanisms of disease in specific cases with SCZ.