Abstract
Social isolation (SI) stress has been recognized as a major risk factor of morbidity in humans and animals, exerting damaging effects at the physical and mental health levels. Posttraumatic stress disorder (PTSD), on the other hand, occurs as a result of experiencing serious, life-threatening, traumatic events and involves involuntary re-experiencing trauma (intrusion), avoidance symptoms, and distortions of cognition and emotional arousal. The literature shows that PTSD is affected by genetic predisposition and triggers a large neurocircuitry involving the amygdala, insula, hippocampus, anterior cingulate- and prefrontal-cortex, and affects the function of the neuroendocrine and immune systems. Social isolation seems to influence the predisposition, onset and outcome of PTSD in humans, whereas it constitutes a valid model of the disorder in animals. According to the PRISMA (preferred reporting items for systematic reviews and meta-analyses) protocol, we systematically reviewed all original studies involving the neurobiological trajectories between SI and PTSD published till July 2019 (database: PubMed/Medline). Out of 274 studies, 10 met the inclusion criteria. We present the results of the retrieved studies in terms of hypothalamic-pituitary-adrenal (HPA)-axis and endocannabinoid system function, immune reactions, neuroplasticity, novel pharmacological targets, and shortening of telomere length, which confirm a synergistic effect on a neurobiological level between the two entities.
Highlights
Posttraumatic stress disorder (PTSD) is a chronic psychiatric condition resulting from direct or indirect exposure to serious trauma and involving intrusive reexperiencing of the traumatic event in the form of unwanted memories, nightmares, flashbacks, emotional and physical distress after exposure to traumatic reminders, persistent avoidance symptoms to trauma-related stimuli, negative alterations of cognitions and mood, as well as marked alterations of arousal and reactivity related to the traumatic event [1].The lifetime prevalence of PTSD in the general population according to the Diagnostic StatisticalManual (DSM)-5 criteria is around 8% with women scoring higher than men [2], whereas the prevalence of the disorder among high-risk groups, like war-veterans, may be four times higher [3]
Brain Sci. 2020, 10, 173 studies have shown that trauma-related disorders are associated with the dysfunctioning of numerous biological systems, and that PTSD symptom severity exerts a cumulative effect on premature aging of the immune system and telomere length [8]
Most of the retrieved studies showed a synergistic effect between PTSD and Social isolation (SI) resembling to an aggravated version of neurobiological findings that comprise the broader PTSD literature as for example the key feature in many of the retrieved papers [45,48,49] concerning the blunting or hypoactivation of HPA-axis, already known from PTSD research [55]
Summary
Posttraumatic stress disorder (PTSD) is a chronic psychiatric condition resulting from direct or indirect exposure to serious trauma (death, threatened death, actual or threatened injury, or sexual violence) and involving intrusive reexperiencing of the traumatic event in the form of unwanted memories, nightmares, flashbacks, emotional and physical distress after exposure to traumatic reminders, persistent avoidance symptoms to trauma-related stimuli, negative alterations of cognitions and mood (dissociative amnesia, negative beliefs about oneself, negative emotional state like fear, horror, guilt and inability of experiencing positive emotions), as well as marked alterations of arousal and reactivity related to the traumatic event (irritability, anger, aggression, self-destructive behavior) [1].The lifetime prevalence of PTSD in the general population according to the Diagnostic StatisticalManual (DSM)-5 criteria is around 8% with women scoring higher than men [2], whereas the prevalence of the disorder among high-risk groups, like war-veterans, may be four times higher [3]. The preparations of the new DSM-5 broadened the criteria to include further emotionally dysregulated states like anger, guilt, shame, and symptoms of derealization and depersonalization, as well as altered self- and other-related conditions and deficits in social cognitions. Such changes gave rise to new neurobiological research challenges [12]. Allo is a positive allosteric modulator of GABA action at GABAA receptors and regulates emotional behavior by exerting anxiolytic, antidepressant, sedative effects It is produced from progesterone in glutamatergic neurons of the cortex, hippocampus and basolateral amygdala through the double enzymatic action of 5α reductase type I (5 α-RI) and 3 α-hydroxysteroid dehydrogenase(3α-HSD) [18,21]. In animal models of PTSD, including the isolated mouse, corticolimbic downregulation of Allo levels correlates to enhanced contextual fear and impaired fear extinction, implying that this neurosteroid may serve as a useful biomarker and treatment option for PTSD across humans and animals [21]
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