[THE ROLE OF STRESS IN MANIC-PSYCHOTIC EPISODE DURING THE TERROR ATTACK OF OCTOBER 7 - CASE REPORT].

INTRODUCTION: The bio-psycho-social model is mostly used to understand the etiology and pathogenesis of psychiatric disorders. Even though in our era, the biological factors became more dominant in the field, the stress-diathesis model is quite acceptable to explain and understand the evolution of psychotic as well as affective disorders. BACKGROUND: In this case report we present a patient, in her late 40's, admitted to our department with a manic-psychotic episode for the first time in her life, after the massive terror attack of October 7, and in which we suggest that the signs and symptoms might be explained using the psycho-dynamic theory. CONCLUSIONS: We conclude suggesting that the equilibrium of the bio-psycho-social model, should be adjusted in the context of time and space, especially during a situation of catastrophic scale in the patient environment. DISCUSSION: Although stress is a risk factor for the development of affective disorders and especially manic-psychotic episodes, there is scarce literature to support it. On the other hand, psycho-dynamic theories sometimes consider stressful life events as a causative factor for the development of depressive as well as manic episodes.

Altered Expression of PDE4 Genes in Schizophrenia: Insights from a Brain and Blood Sample Meta-Analysis and iPSC-Derived Neurons.

Schizophrenia symptomatology includes negative symptoms and cognitive impairment. Several studies have linked schizophrenia with the PDE4 family of enzymes due to their genetic association and function in cognitive processes such as long-term potentiation. We conducted a systematic gene expression meta-analysis of four PDE4 genes (PDE4A-D) in 10 brain sample datasets (437 samples) and three blood sample datasets (300 samples). Subsequently, we measured mRNA levels in iPSC-derived hippocampal dentate gyrus neurons generated from fibroblasts of three groups: healthy controls, healthy monozygotic twins (MZ), and their MZ siblings with schizophrenia. We found downregulation of PDE4B in brain tissues, further validated by independent data of the CommonMind consortium (515 samples). Interestingly, the downregulation signal was present in a subgroup of the patients, while the others showed no differential expression or even upregulation. Notably, PDE4A, PDE4B, and PDE4D exhibited upregulation in iPSC-derived neurons compared to healthy controls, whereas in blood samples, PDE4B was found to be upregulated while PDE4A was downregulated. While the precise mechanism and direction of altered PDE4 expression necessitate further investigation, the observed multilevel differential expression across the brain, blood, and iPSC-derived neurons compellingly suggests the involvement of PDE4 genes in the pathophysiology of schizophrenia.