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NEUROGENOMICS

Modeling PTSD neuronal stress responses in a dish

Nature Neuroscience volume 25, pages 1402–1404 (2022)Cite this article

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How genetic and environmental risk factors interact to trigger the development of post-traumatic stress disorder (PTSD) remains largely unknown. Seah et al. model stress hypersensitivity as a potential mechanism by examining transcriptomic responses to glucocorticoids in neurons derived from individuals with PTSD.

PTSD occurs in some individuals who undergo direct exposure to intense and terrifying experiences such as combat. Genetic studies of PTSD, especially large-scale genome-wide association studies (GWASs), are starting to reveal genetic variations that predispose an individual to develop PTSD1,2. However, the molecular and cellular mechanisms that explain individual susceptibility to PTSD remain largely unknown, which hinders risk prediction and more tailored treatment of PTSD. A major challenge is that, like other neuropsychiatric disorders, PTSD risk is polygenic, probably involving hundreds of genes each with a small effect. Moreover, many disease risk genes may elicit their biological effects only upon exposure to environmental risk factors, such as stress. It is imperative to develop a human cell-based model for dissecting the complex neurobiological mechanisms that underlie PTSD and other stress-related psychiatric conditions.

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Fig. 1: Modelling PTSD gene–environment interactions using PBMCs and iPS cell-derived glutamatergic NGN2-induced neurons.

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Authors and Affiliations

  1. Center for Psychiatric Genetics, NorthShore University HealthSystem, Evanston, IL, USA

    Siwei Zhang, Alan R. Sanders & Jubao Duan

  2. Department of Psychiatry and Behavioral Neuroscience, University of Chicago, Chicago, IL, USA

    Siwei Zhang, Alan R. Sanders & Jubao Duan

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  1. Siwei Zhang
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  2. Alan R. Sanders
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  3. Jubao Duan
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Correspondence to Jubao Duan.

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Zhang, S., Sanders, A.R. & Duan, J. Modeling PTSD neuronal stress responses in a dish. Nat Neurosci 25, 1402–1404 (2022). https://doi.org/10.1038/s41593-022-01172-9

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