A similar fractionation of mechanisms that contribute to psychiat

A similar fractionation of mechanisms that contribute to psychiatric diseases might be achieved by state and trait mapping, based on psychopathological and personality models. The ultimate hope is that the better understanding of the biological pathways to psychiatric disease will result in the development of new treatments. The insight into the neural mechanisms of psychiatric symptoms achieved through neuroimaging has already informed new nonpharmacological interventions such as deep-brain stimulation, transcranial magnetic stimulation, and neurofeedback that are currently

in clinical testing. Early and prophylactic interventions present an emerging future direction in clinical psychiatry (McGorry et al., 2011), and neuroimaging has the potential to aid the identification of learn more individuals at risk and monitor the effects of these

Galunisertib interventions. Future aims in the development of surrogate treatment markers would involve assessing whether psychological or pharmacological interventions normalize the patterns of brain structure or function that predicted disease risk. Another future direction with considerable clinical benefit would be the development of biomarkers that predict the response to a particular treatment and could then be used for therapeutic stratification. Despite available imaging techniques (Table 1) and molecular targets (Table 2), new ways of targeting intracellular processes are likely needed. A key persisting question for imaging research in psychiatry with respect to developing novel treatments is whether to focus on the detection of the primary pathology, or whether to probe the pathways that underlie resilience and recovery.

There is thus ample scope for ongoing and new psychiatric imaging initiatives to establish biomarkers and targets for diagnostic and therapeutic applications. The author’s work was supported by grants from the Biotechnology and Biological Sciences Research Council (BBSRC) (BB/G021538), the Economic and Social Research Council (ESRC) (RES-062-23-0946), and the Welsh National Centre for Mental Health. Lorraine Woods provided invaluable help designing the figures, and Miles through Cox, Stephen Daniels, Rainer Goebel, Tom Lancaster, Niklas Ihssen, Matthias Munk, Michael O’Donovan, Christian Röder, Krish Singh, Richard G Wise, and Kenneth Yuen commented on earlier versions of the manuscript or provided answers to specific questions. “
“The GABAergic system of the mammalian brain consists of GABA-releasing cells and receptors that bind GABA. GABA-releasing cells are extraordinarily diverse and highly specialized (Freund and Buzsáki, 1996 and Klausberger and Somogyi, 2008), both controlling the activity of local networks (e.g., interneurons) and forming the output of some brain areas and nuclei (e.g., striatal medium spiny neurons and cerebellar Purkinje cells).

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