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BACKGROUND: The number of individuals diagnosed with Alzheimer's disease (AD) has increased, and it is estimated to continue rising in the coming years. The diagnosis of this disease is challenging due to variations in onset and course, its diverse clinical manifestations, and the indications for measuring deposit biomarkers. Hence, there is a need to develop more precise and less invasive diagnostic tools. Multiple studies have considered using electroencephalography (EEG) entropy measures as an indicator of the onset and course of AD. Entropy is deemed suitable as a potential indicator based on the discovery that variations in its complexity can be associated with specific pathologies such as AD. METHODOLOGY: Following PRISMA guidelines, a literature search was conducted in 4 scientific databases, and 40 articles were analyzed after discarding and filtering. RESULTS: There is a diversity in entropy measures; however, Sample Entropy (SampEn) and Multiscale Entropy (MSE) are the most widely used (21/40). In general, it is found that when comparing patients with controls, patients exhibit lower entropy (20/40) in various areas. Findings of correlation with the level of cognitive decline are less consistent, and with neuropsychiatric symptoms (2/40) or treatment response less explored (2/40), although most studies show lower entropy with greater severity. Machine learning-based studies show good discrimination capacity. CONCLUSIONS: There is significant difficulty in comparing multiple studies due to their heterogeneity; however, changes in Multiscale Entropy (MSE) scales or a decrease in entropy levels are considered useful for determining the presence of AD and measuring its severity.

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Background: The Behavioral Inhibition System (BIS) comprises limbic circuitry implicated in avoidance behaviors. Its increased activation has been identified as a risk factor for anxiety and depressive disorders. In addition, both Catechol-O-Methyltransferase (COMT) and Brain Derived Neurotrophic Factor (BDNF) have been postulated as candidate genes that constitute a vulnerability for the onset of anxiety and depressive disorders. The aim of this study was to evaluate the possible association between the rs4680 polymorphism of the COMT gene and the rs6265 polymorphism of the BDNF gene with the BIS and the Behavioral Activation System (BAS) in a population sample from Colombia. Methods: Genetic information was obtained by extracting DNA from blood samples of 80 participants and using Taqman probes designed for each polymorphism. In addition, participants completed a BIS/BAS scale in order to establish a neuropsychological classification. Results: The frequency of the Met allele of the BDNF gene was greater in the group with BIS sensitivity compared to the group with BAS sensitivity. On the contrary, the frequency of the Met allele of the COMT gen did not show a significant association with the BIS. Conclusions: The rs6265 polymorphism of BDNF gene is associated with the BIS which in turn constitutes a risk factor for anxiety and depression.

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Psychological detachment is the central experience of recovery from work-related stress that allows individuals to reduce burnout symptoms. The stressor-detachment model (SDM) contends that job resources moderate the relationship between job stressors and psychological detachment. We designed an instrument to measure job resources from a multidimensional perspective. A sample of n = 394 individuals from the health service industry participated in the study. Data indicate that job resources comprise a four-factor structure underlying a formative model. Consistent with the SDM, a partial least squares structural equation modeling (PLS-SEM) analysis suggests a moderating effect of job resources (e.g., control over working conditions, leaders' emotional support), between work intensification and psychological detachment. In addition; results indicate that workers who perceive high levels of support from their organization achieved higher levels of detachment compared with those who perceived low levels of support. Theoretical as well as practical implications for stress management practices, occupational health, and well-being are discussed.

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En la actualidad, existen tratamientos eficaces para reducir los síntomas de ansiedad y el malestar asociado. Sin embargo, se observa con frecuencia que las respuestas de ansiedad, después de haberse extinguido, se recuperan, sin que esté claro el mecanismo que subyace a dicha recuperación. Desde hace décadas, se considera la posibilidad de un mecanismo de reconsolidación que colaboraría en el proceso de almacenar nuevamente los recuerdos que han sido evocados. Algunas investigaciones recientes revelan que la intervención sobre el mecanismo de reconsolidación aparentemente previene la recuperación de respuestas de ansiedad que han sido previamente extinguidas. Si esto es así, podría ser una alternativa a los tratamientos actuales de los trastornos de ansiedad basados en la exposición. El objetivo del presente trabajo es revisar la evidencia sobre los efectos de actuar sobre el mecanismo de reconsolidación para la reducción de las respuestas de ansiedad. Finalmente se discuten las posibles implicaciones clínicas.

At the present, effective treatments are available to reduce anxiety symptoms and their associated distress. Nevertheless, it is frequently observed that anxiety responses are recovered after extinction, without being clear the responsible mechanism of such phenomenon. For decades, it has been presumed the existence of a reconsolidation mechanism. Such mechanism is thought to participate in the re-storage of memories that have been evoked. Recent research apparently reveals that intervention on reconsolidation mechanisms prevents the recovery of anxiety responses that have been previously extinguished. Intervention on these mechanisms could represent an alternative to current psychological treatments for anxiety disorders based on exposure procedures. The objective of the present work is to review the evidence on reconsolidation mechanisms and its effects on the reduction of anxiety responses. Finally some clinical implications will be discussed.

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