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Max Planck Institute of Psychiatry, Munich, Germany
Mathias V. Schmidt is a group leader at the Department of Stress Neurobiology and Neurogenetics at the Max Planck Institute of Psychiatry in Munich (Germany). His scientific aim is to pursue the question of why some individuals are resilient to severe stress exposure and thrive even in the face of adversity.
The Schmidt Laboratory investigates the interplay of genetic predisposition and early experiences during different stages of development in shaping stress resilience. Their research areas include stress-related psychiatric disorders as well as the connection between the brain stress system and metabolic (dys)regulation. By combining state-of-the-art behavioral, neuroendocrine and molecular readouts, they aim to develop novel pharmacological or genetic approaches to modulate, reverse or even prevent individual stress vulnerability. Recent interest also includes the impact of the prolonged COVID-19 pandemic on stress resilience and mental health.
One of the lab’s achievements is identifying FKBP51 as a potential molecular link that may drive the stress risk for disease. The experiments confirmed that the protein indeed links stress response with an increased risk for metabolic disorders. Therefore, the findings can be used to develop a drug that can then be tested on humans.
Mathias V. Schmidt received his PhD in 2004 at the University of Leiden (Netherlands) for his work on the mechanisms of early life stress in mice. He subsequently completed a postdoc at the Max Planck Institute of Psychiatry, Germany where he also received his habilitation in 2010.
The increasing rate of stress-related disorders, with mood disorders as major depression leading the way, and the social and well as economic consequences of these illnesses represent a growing threat to our society. A dysregulation of the body’s main stress system, the hypothalamic-pituitary-adrenal axis, is a major hallmark of depression, but so far no specific treatments tackling this mechanism are available. It seems clear that genetic predispositions interact with environmental demands such as chronic stress and modulate the long-term health outcome. In addition, there is abundant evidence that environmental circumstances early in life are capable of shaping the adult phenotype. Here I will discuss two aspects that can shape stress resilience: genetic predisposition and experiences during early life. Firstly, I will focus on the co-chaperone FK506-binding protein 51 (FKBP51) as a very promising target molecule for new drug therapies, as it is highly linked to stress-related human disorders, directly regulates stress hormone activity and metabolic disturbances. Secondly, I will address the influence of the early life environment on later stress resilience or vulnerability dependent on genetic background. Taken together, our results now pave the way for tailored and specific treatment strategies that could be beneficial for improving stress resilience in health and disease.
de Kloet, E.R., Sibug, R.M., Helmerhorst, F.M., Schmidt, M., 2005. Stress, genes and the mechanism of programming the brain for later life. Neurosci. Biobehav. Rev. 29, 271–281.
Balsevich, G., Häusl, A.S., Meyer, C.W., Karamihalev, S., Feng, X., Pöhlmann, M.L., Dournes, C., Uribe-Marino, A., Santarelli, S., Labermaier, C., Hafner, K., Mao, T., Breitsamer, M., Theodoropoulou, M., Namendorf, C., Uhr, M., Paez-Pereda, M., Winter, G., Hausch, F., Chen, A., Tschöp, M.H., Rein, T., Gassen, N.C., Schmidt, M. V, 2017. Stress-responsive FKBP51 regulates AKT2-AS160 signaling and metabolic function. Nat. Commun. 8, 1725.
Karamihalev, S., Brivio, E., Flachskamm, C., Stoffel, R., Schmidt, M. V, Chen, A., 2020. Social dominance mediates behavioral adaptation to chronic stress in a sex-specific manner. Elife 9.
Vinkers, C.H., van Amelsvoort, T., Bisson, J.I., Branchi, I., Cryan, J.F., Domschke, K., Howes, O.D., Manchia, M., Pinto, L., de Quervain, D., Schmidt, M. V, van der Wee, N.J.A., 2020. Stress resilience during the coronavirus pandemic. Eur. Neuropsychopharmacol. 35, 12–16.