Publications by authors named "Bonapersona"

Stress initiates a cascade of (neuro)biological, physiological, and behavioral changes, allowing us to respond to a challenging environment. The human response to acute stress can be studied in detail in controlled settings, usually in a laboratory environment. To this end, many studies employ acute stress paradigms to probe stress-related outcomes in healthy and patient populations.

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Article Synopsis
  • The study examines how acute stress activates different brain networks and which specific cells change their activity over time.
  • A processing pipeline was created to analyze immediate early gene expression in response to a foot shock, providing insights at both functional network and single-cell levels in 3D.
  • Results showed that most brain regions became more active post-stress, with the hypothalamus reacting the fastest, while c-fos+ cell density varied over time, indicating distinct patterns of cellular response among different brain areas.
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Early-life adversity (ELA) causes long-lasting structural and functional changes to the brain, rendering affected individuals vulnerable to the development of psychopathologies later in life. Immediate-early genes (IEGs) provide a potential marker for the observed alterations, bridging the gap between activity-regulated transcription and long-lasting effects on brain structure and function. Several heterogeneous studies have used IEGs to identify differences in cellular activity after ELA; systematically investigating the literature is therefore crucial for comprehensive conclusions.

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Article Synopsis
  • Low statistical power in animal research makes findings less reliable, and increasing sample sizes poses ethical and practical challenges.
  • Using Bayesian priors from historical control data can significantly reduce the needed sample size or increase the power of studies without needing more animals.
  • The open-source tool, RePAIR, was developed to implement this method, validated with data from seven rodent studies on early-life adversity, enhancing the reliability of animal research outcomes.
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One of the features of the Consortium on Individual Development is the existence of a rodent cohort, in parallel with the human cohorts. Here we give an overview of the current status. We first elaborate on the choice of rat and mouse models mimicking early life adverse or beneficial conditions during development.

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Early life stress (ELS) is considered a major risk factor for developing psychopathology. Increasing evidence points towards sex-dependent dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis as a contributing mechanism. Additionally, clinical studies suggest that the mineralocorticoid receptor (MR) may further confer genetic vulnerability/resilience on a background of ELS.

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Altered cognitive performance is considered an intermediate phenotype mediating early life adversity (ELA) effects on later-life development of mental disorders, e.g. depression.

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Adverse early life events are a well-established risk factor for the precipitation of behavioral disorders characterized by anomalies in the dopaminergic system, such as schizophrenia and addiction. The correlation between early life conditions and the dopaminergic system has been causally investigated in more than 90 rodent publications. Here, we tested the validity of the hypothesis that early life stress (ELS) alters dopamine signaling by performing an extensive 3-level mixed effect meta-analysis.

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