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. 2024 Nov;50(1):318-319.
doi: 10.1038/s41386-024-01953-9.

Multisystem stress response biotypes: a precision psychiatry approach to identifying and treating multidimensional risk factors for anhedonia in adolescence

Danielle S Roubinov  1 , Aysenil Belger  2
Affiliations

Multisystem stress response biotypes: a precision psychiatry approach to identifying and treating multidimensional risk factors for anhedonia in adolescence

Danielle S Roubinov et al. Neuropsychopharmacology. 2024 Nov.

Erratum in

No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Conceptual Model of Multisystem Stress Response Biotypes: acute stress activates neural and physiological systems critical for the onset and regulation of adaptive stress responses.
Neural Regulators: Coordinated prefrontal cortex, hippocampus, and amygdala activation works together to regulate the acute stress response. This coordinated activity of prefrontal (PFC), hippocampal (Hipp), and amygdala (Amyg) systems ensures that the stress response is appropriate to the situation and that the body can return to a state of balance once the stressor is no longer present. The amygdala detects threats and initiates the stress response, the hippocampus provides contextual information and feedback to regulate the HPA axis (hypothalamus -Hyp and ventral striatum – VS), and the prefrontal cortex helps to assess the situation, plan responses, and inhibit excessive emotional reactions. Physiological Regulators: Coordinated activation of the Autonomic Nervous System (ANS) through its Parasympathetic and Sympathetic arms (PSN and SNS, respectively) and the HPA (hypothalamic-pituitary-adrenal Axis) has been associated with multiple stress response profiles, including the ACM-derived Buffered profile, marked by greater activation of the PNS, a Vigilant Profile, marked by hyperactivation of the HPA, and a Sensitive Profile, marked by greater activation of the HPA and low/moderate ANS activity. Balancing and Coordinating Activation: The neural and physiological systems are highly interdependent and interlinked: The hippocampus and PFC provide feedback to the HPA axis to modulate and eventually terminate the stress response. High levels of cortisol signal the hippocampus to inhibit further activation of the HPA axis, while the PFC helps to re-evaluate the stressor and diminish the emotional response. The PFC further helps to balance the activation of the amygdala and the stress response. Under acute stress, the PFC can help to downregulate the amygdala’s activity, reducing the overall stress response. The Multisystem Stress Response Biotypes Model posits that dysregulation in the coordination between these stress systems differentially modulates risk for anhedonia and may represent early risk markers for targeted early interventions. Arrow thickness represents relative strength of activation of individual systems leading to distinct profiles as in Glier et al. [6].
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