Anti-stress Properties of Atypical Antipsychotics

Abstract

Stress exposure represents a major environmental risk factor for schizophrenia and other psychiatric disorders, as it plays a pivotal role in the etiology as well as in the manifestation of disease symptomatology. It may be inferred that pharmacological treatments must be able to modulate the behavioral, functional, and molecular alterations produced by stress exposure to achieve significant clinical outcomes. This review aims at examining existing clinical and preclinical evidence that supports the ability of atypical antipsychotic drugs (AAPDs) to modulate stress-related alterations. Indeed, while the pharmacodynamic differences between AAPDs have been extensively characterized, less is known on their ability to regulate downstream mechanisms that are critical for functional recovery and patient stabilization. We will discuss stress-related mechanisms, spanning from neuroendocrine function to inflammation and neuronal plasticity, which are relevant for the manifestation of schizophrenic symptomatology, and we will discuss if and how AAPDs may interfere with such mechanisms. Considering the impact of stress in everyday life, we believe that a better understanding of the potential effects of AAPDs on stress-related mechanisms may provide novel and important insights for improving therapeutic strategies aimed at promoting coping mechanisms and enhancing the quality of life of patients affected by psychiatric disorders.

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“…However, it should be mentioned that the design of our experiments allowed us to report only a single time point of IEGs induction by drug treatment. Further studies should investigate the effects of a chronic administration of the compound and particularly in animal models that reproduce specific etiological mechanisms of schizophrenia [ 50 ]. Interestingly, it has been recently demonstrated that chronic treatment with the selective TAAR1 partial agonist RO5263397 ameliorated chronic stress-induced changes in cognitive function [ 51 ], suggesting that this receptor mechanism in SEP-856 may produce long-term changes aimed at correcting the dysfunction of key psychopathologic domains.…”

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“…In contrast to fentanyl, which interacts primarily with μ-opioid receptors, oxycodone acts at multiple opioid receptors including κ-opioid receptors [ 44 ]; κ-opioid receptor agonists may offer some neuroprotection in brain ischemia [ 45 ]. Although typical antipsychotics can impede neurorecovery [ 46 ], atypical antipsychotics (such as quetiapine) may confer antiinflammatory and neuroprotective benefits [ 47 , 48 ]. A recent retrospective matched cohort study demonstrated decreased mortality and improved neurologic outcomes in critically ill patients with traumatic brain injury who received low-dose quetiapine [ 49 ].…”

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