Have you ever found yourself scrolling on your phone even when a deadline is approaching, reassuring yourself that “starting tomorrow is still fine”? For most people, procrastination is regarded as a maladaptive habit that can be corrected.
However, for some individuals, procrastination becomes persistent, uncontrollable, and is accompanied by significant distress and anxiety. This subclinical condition is referred to as psychopathological procrastination.
Led by Prof. ZHOU Yuan from the Institute of Psychology, Chinese Academy of Sciences and Prof. CHEN Zhiyi from the School of Psychology, Third Military Medical University, a research team systematically investigated the underlying neurobiological mechanisms of psychopathological procrastination from a psychopathological perspective.
The study recruited 142 same-sex twins (71 twin pairs). First, twin modeling revealed that psychopathological procrastination exhibited moderate heritability (h² = 0.47), indicating a substantial genetic contribution. Next, the researchers applied normative modeling trained on a large ENIGMA lifespan dataset (N ≈ 37,407) to project individual brain morphology onto population-based developmental trajectories, yielding region-specific deviation scores. Longitudinal analyses showed that morphological deviations in the nucleus accumbens (NAcc) during adolescence significantly predicted adult psychopathological procrastination. More importantly, bivariate genetic modeling demonstrated that this association was largely driven by shared genetic factors. Deviations in the right NAcc were not only phenotypically correlated with procrastination (rph = 0.18), but also exhibited a remarkably strong genetic correlation (rg = 0.89).
To further characterize whole-brain patterns, the researchers employed inter-subject representational similarity analysis to construct neural and behavioral representational dissimilarity matrices. The resulting brain-wide representational map revealed that procrastination-related deviations were primarily localized within the default mode network. These neural patterns were spatially aligned with the cortical functional gradient and also enriched in key dopaminergic (DAT/D1) and serotonergic (5-HT receptors) neurotransmitter systems.
Finally, the team integrated neuroimaging features with human brain transcriptomic data through spatial gene-brain mapping and developmental trajectory profiling. The results revealed significant associations with molecular transport processes, neuroimmune responses, and neuroinflammatory pathways, further implicating dysregulation of dopamine and serotonin signaling.
Overall, the study delineates a multi-system neurogenetic architecture of psychopathological procrastination. Adolescent neurodevelopmental deviations serve as early neural fingerprints of later procrastination risk, supported by shared genetic influences and molecular pathways involving reward processing and neuroimmune regulation. These findings also offer new insights into the early identification and stratified intervention of psychopathological procrastination, suggesting that brain developmental “deviation signatures” in adolescence may provide objective biomarkers for educational and mental health services.
This work was published in Molecular Psychiatry on Jan. 8 and was supported by the National Natural Science Foundation of China (32300907, 72033006), the Chongqing Natural Science Foundation (CSTB2025NSCQ-GPX0570), and the AMU-RD Scholar Foundation (202211001).
