Publications by authors named "Gustavo Tafet"

Understanding the impact of stress on cognitive processes, particularly decision-making, is crucial as it underpins behaviors essential for survival. However, research in this domain has yielded disparate results, with inconsistencies evident across stress-induction paradigms and drug administration protocols designed to investigate specific stress pathways or neuromodulators. Building upon empirical studies, this research identifies a multifaceted matrix of variables contributing to the divergent findings.

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Aphantasia has been described as the inability to voluntarily evoke mental images using the "mind's eye." We studied a congenital aphantasic subject using neuropsychological testsand 64 channel EEG recordings, in order to studycortical activity involved in perception and imagery evaluating event-related potentials(N170, P200, N250). The subject is in the normal range of the neuropsychological tests performed, except for specific imagery tests.

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Stress in general, and early life stress in particular, has been associated with the development of anxiety and mood disorders. The molecular, biological and psychological links between stress exposure and the pathogenesis of anxiety and mood disorders have been extensively studied, resulting in the search of novel psychopharmacological strategies aimed at targets of the hypothalamic-pituitary-adrenal (HPA) axis. Hyperactivity of the HPA axis has been observed in certain subgroups of patients with anxiety and mood disorders.

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The role of stress in the origin and development of depression may be conceived as the result of multiple converging factors, including the chronic effect of environmental stressors and the long-lasting effects of stressful experiences during childhood, all of which may induce persistent hyperactivity of the hypothalamic-pituitary-adrenal axis. These changes, including increased availability of corticotropin-releasing factor and cortisol, are also associated with hyperactivity of the amygdala, hypoactivity of the hippocampus, and decreased serotonergic neurotransmission, which together result in increased vulnerability to stress. The role of other monoaminergic neurotransmitters, genetic polymorphisms, epigenetic mechanisms, inflammatory processes, and altered cognitive processing has also been considered in the development of a comprehensive model of the interactions between different factors of vulnerability.

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The aim of this study was to evaluate the efficacy of cognitive therapy (CT) in the treatment of generalized anxiety disorder (GAD), as it would be reflected through both psychological and psychoneuroendocrinological parameters. For this purpose, a group of outpatients with GAD were treated with CT for up to a maximum of 24 sessions. In order to assess psychological and biological changes, anxiety-related symptoms were evaluated according to the Hamilton Anxiety Rating Scale (HAM-A), and the hypothalamic-pituitary-adrenal (HPA) function was determined through assessment of circulating cortisol levels.

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The adaptive response to stress is characterized by activation of neural and neuroendocrine cascades mediated mainly by the noradrenergic/sympathetic and limbic-hypothalamic-pituitary-adrenal (HPA) systems, respectively. Chronic psychosocial stress has long been associated with the origin and development of depression, where increased levels of cortisol have been observed in both conditions. In this regard, increased levels of cortisol could be directly involved in the mood changes observed in depression, and direct connections between these and alterations of the serotonergic neurotransmission have been also proposed.

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Objective: The goal of this report is to develop a comprehensive model, which integrates psychosocial and neurobiological aspects, for better understanding the link between chronic stress and mood disorders.

Method: A selective review of the relevant bibliography was conducted. The significant data were integrated with clinical and preclinical findings, particularly focusing on the effect of the hypothalamo-pituitary-adrenal (HPA) activity on the serotonergic neurotransmission in the CNS.

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