Background Procrastination describes irrational delays of scheduled tasks despite clear awareness of adverse consequences to do so. Although procrastination is well-known to be linked to psychiatric or pathological processes, insights into why procrastination may contribute to psychopathological outcomes has not been fully explored. The aim of the current study was to identify the criterion for “pathological procrastination” and its preclinical correlates. Methods This is a longitudinal and prospective observational study with a five-year interval. Participants ( N = 464) completed measures of trait procrastination in November 2018, with a follow-up conducted in March 2023 ( N = 267) to collect preclinical psychiatric symptoms via self-reported measures. A constrained multivariate direct gradient model (cmDGM) was built to prospectively fit procrastination to the preclinical psychiatric symptomatology that formulated by DSM-5 framework. The 2-stage psychopathological connectome model was further constructed to constitute a “diagnostic criterion” reflecting “pathological procrastination”. Results Procrastination prospectively predicted severe preclinical psychiatric symptoms and unhealthy lifestyles. Preclinical bridge hubs of “failure to self-regulate delays”, “failure to control adverse consequences”, “useless to self-change”, “out-of-control irruptions”, “poor sleep quality” and “negative emotional reactions” were captured for highly local and global disruptions in the psychopathological network of procrastination, and thus constituted the 9-item pathological procrastination diagnostic criterion (3PDC) with good diagnostic performance (AUC = 0.82, p <.01). Conclusions The present study revealed the predictive rol of procrastination for preclinical psychiatric symptomatology, and further established the preclinical 3PDC to lay the foundation for the “diagnostics of pathological procrastinators” by both quantitative measurements and DSM-structured binary schemes.

Background Social deficits and dysregulations in dopaminergic midbrain-striato-frontal circuits represent transdiagnostic symptoms across psychiatric disorders. Animal models suggest that modulating interactions between the dopamine and renin-angiotensin system with the angiotensin receptor antagonist Losartan (LT) can modulate learning and reward-related processes. We have therefore determined the behavioral and neural effects of LT on social reward and punishment processing in humans. Methods A pre-registered randomized double-blind placebo-controlled between-subject pharmacological design was combined with a social incentive delay fMRI paradigm during which subjects could avoid social punishment or gain social reward. Healthy volunteers received a single-dose of LT (50mg, n=43) or placebo (n=44). Reaction times and emotional ratings served as behavioral outcomes, on the neural level activation, connectivity and social feedback prediction errors were modelled. Results Relative to placebo, LT switched reaction times and arousal away from prioritizing punishment towards social reward. On the neural level the LT-enhanced motivational salience of social rewards was accompanied by stronger ventral striatum-prefrontal connectivity during reward anticipation and attenuated activity in the ventral tegmental area (VTA) and associated connectivity with the bilateral insula in response to punishment during the outcome phase. Computational modelling further revealed an LT-enhanced social reward prediction error signal in VTA and dorsal striatum. Conclusions LT shifted motivational and emotional salience away from social punishment towards social reward via modulating distinct core nodes of the midbrain-striato-frontal circuits. The findings document a modulatory role of the renin-angiotensin system in these circuits and associated social processes, suggesting a promising treatment target to alleviate social dysregulations.