Mental disorders develop over the lifespan. As trivial as this statement may sound, as complicated are its implications. Disorders that are commonly considered to have their onset in adulthood often feature precursors in childhood or adolescence, e.g., depression can be preceded by anxiety disorders in infancy. In addition, we know by now that “typical” childhood disorders such as ADHD and autism persist into adulthood, but change clinical presentation considerably. Genetic factors have an important role in shaping this developmental trajectory and these may not only include classical common and rare genetic variants, that can easily be measured in bodily fluids, but also de novo germline and somatic mutations which might only be detectable in the brain. During brain development, which takes place until the 20s, a number of risk factors may occur: pre- and postnatal famine, viral infections, delivery complications, drug exposure, to name but a few. Beyond these biological mechanisms, of course also varying environmental influences affect the course of disease; traumatic life events, familial atmosphere and parenting style, socioeconomic stratum all may shape the progression of disorder (or, on the other hand, resilience against it). All of these factors (Fig. 1) interact—for instance, initial studies point to an interaction of risk gene variants with traumatic life events to increase the risk towards later-life depression and anxiety disorders. Importantly, all processes ultimately converge on the level of the brain where a dynamic landscape of neural function and structure is mirroring a highly adaptive and plastic genomic–transcriptomic network of the neuron.
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