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Major programs in psychiatric genetics have identified 4150 risk loci for psychiatric disorders. These loci converge on a small\ud number of functional pathways, which span conventional diagnostic criteria, suggesting a partly common biology underlying\ud schizophrenia, autism and other psychiatric disorders. Nevertheless, the cellular phenotypes that capture the fundamental features\ud of psychiatric disorders have not yet been determined. Recent advances in genetics and stem cell biology offer new prospects for\ud cell-based modeling of psychiatric disorders. The advent of cell reprogramming and induced pluripotent stem cells (iPSC) provides\ud an opportunity to translate genetic findings into patient-specific in vitro models. iPSC technology is less than a decade old but holds\ud great promise for bridging the gaps between patients, genetics and biology. Despite many obvious advantages, iPSC studies still\ud present multiple challenges. In this expert review, we critically review the challenges for modeling of psychiatric disorders, potential\ud solutions and how iPSC technology can be used to develop an analytical framework for the evaluation and therapeutic\ud manipulation of fundamental disease processes.

The amino-acid N-acetyl-aspartate (NAA) is located in neurons and the concentration of NAA correlates with neuronal mitochondrial function. The signal of NAA, as measured with proton magnetic resonance spectroscopy (1H-MRS), is considered to reflect both, neuronal density and integrity of neuronal mitochondria. A reduction of the NAA concentrations has been found in several psychiatric disorders. Newer studies report reversal of decreased NAA concentration with treatment. The objective of this review is to summarize the literature on NAA changes in association with psychopharmacological treatment in psychiatric disorders (affective disorders, obsessive-compulsive disorder, schizophrenia and dementia). The majority of studies identified increased NAA concentrations in response to treatment, while a smaller number of studies did not find this effect. The NAA increase seems to be neither specific for a certain disorder nor for a specific intervention. This suggests that the reduction of NAA may represent an altered functional (metabolic) state of neurons common to different psychiatric disorders and the increase after treatment to indicate functional restoration as one general effect of interventions.