Abstract
While general procrastination is common, psychopathological procrastination, a debilitating phenotype often indicative of subclinical psychiatric conditions, remains poorly understood in terms of its neurobiological underpinning. Challenging its traditional conceptualization as a mere behavioral deficit, we investigated the neurogenetic architecture of psychopathological procrastination. Leveraging a prospective adolescent twin cohort (N = 71 twin pairs) with neuroanatomical imaging (baseline) and psychopathological procrastination phenotyping in young adulthood (8-year follow-up), we first established moderate heritability for psychopathological procrastination (h² = 0.47, 95% CI: 0.14 - 0.71). Employing normative modeling of brain morphology, we found that adolescent neurodevelopmental deviations, specifically within the nucleus accumbens (NAcc), predicted adult psychopathological procrastination. Crucially, these predictive adolescent NAcc deviations exhibited a strong shared genetic basis with adult psychopathological procrastination (rg = 0.89, 95% CI: 0.89 - 1.00). Beyond regional effects, psychopathological-procrastination-specific whole-brain deviation patterns were identified, which showed neurobiological enrichment with cortical functional gradient and key dopaminergic (DAT/D1) and serotonergic (5-HT receptors) neurotransmitter systems. Both cross-sectional and longitudinal transcriptomic integration of these neuroimaging signatures with human brain gene expression data pinpointed significant associations with molecular transport, neuroimmune responses, and neuroinflammation, further implicating dysregulation within serotonergic and dopaminergic pathways. Collectively, our findings delineate a multisystem neurogenetic architecture of psychopathological procrastination, providing supportive evidence that recontextualizes this debilitating phenotype from a simple behavioral issue to a condition with neurodevelopmental antecedents, potentially suggesting its conceptualization as a subclinical brain disorder.
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Data availability
Data supporting reproducibility of this study are available in the main text and the supplementary materials. Data for neuroimaging normative modeling derives from ENIGMA Consortium Lifespan Working Group (https://enigma.ini.usc.edu/). Data for macroscale brain phenotype are curated by Neuromap (https://github.com/netneurolab/neuromaps). Data for supporting overrepresentation analysis (ORA) and neurobiological enrichment analysis are generated from Metascape (https://metascape.org/gp/index.html) and GAMBA (http://dutchconnectomelab.nl/GAMBA/) databases, respectively. Gene expression data are constructed from Allen Human Brain Atlas (AHBA) (https://human.brain-map.org/static/) and BrainSpan (Atlas of the Developing Human Brain) (https://www.brainspan.org/). The raw genetic neuroimaging data are available under restricted access for data legal restrictions. Specifically, these genetic neuroimaging data are collected by the Beijing Twin Data Collection Project, which has not yet completed. Thus, given biometric data that are undergoing collection in an ongoing project, the legal censorship to share them from data regulation authorities is not available at this time, until this project is fully completed. For scientific collaborations or research purposes, any researchers can obtain access by reaching out Dr. Yuan Zhou (zhouyuan@psych.ac.cn).
Code availability
No custom codes are central in analyzing data. Neuroimaging normative modeling has been conducted via online tool (CentileBrain, https://centilebrain.org). Spatial alignment to map whole-brain deviation pattern into brain phenotype is implemented by Neuromap (https://github.com/netneurolab/neuromap). Visualization to brain maps capitalizes on R packages “ggseg” (https://ggseg.github.io/ggseg/) and its derivatives, such as “ggsegSchaefer”(https://github.com/ggseg/ggsegSchaefer). Schematic diagram for the theoretical model is generated by Biorender (Trial version).
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Acknowledgements
We do appreciate Dr. Xuerong Liu for assistance on proofreading and thank to Prof. Tingyong Feng for scientific comments on theoretical conceptualization. We are sincerely thankful to Dr. Runsen Chen and Dr. Diyang Qu for their comments and suggestions to improve writing quality.
Funding
National Natural Science Foundation of China (32300907, 72033006, CZY, ZY). Chongqing Natural Science Foundation (CSTB2025NSCQ-GPX0570, General Project, CZY). PLA Talent Program Foundation (2022160258, CZY). AMU-RD Scholar Foundation (202211001, CZY).
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Conceptualization and Writing—original draft: HYY, YCT, CZY. Methodology: HYY, ZD, JYN. Investigation: HYY, FQC. Visualization: CZY, HYY, LW. Supervision: CZY, ZY, JKB. Writing—review & editing: JKB, LW, ZY, CZY.
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All methods were performed in accordance with the ethical standards of the 1964 Declaration of Helsinki and its later amendments (most recently, the 2013 revision). The study protocol and analytic pipeline were officially approved by the Institutional Review Board (IRB) of the Institute of Psychology (Chinese Academy of Sciences, China, #H20037) and the IRB of the Faculty of Psychology (Southwest University, China, #H24121). Informed consent was obtained from all the human participants prior to their involvement in the study. This study does not involve any other live vertebrates (animals).
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Hu, Y., Tang, Y., Li, W. et al. Shared neurogenetic architecture links adolescent neurodevelopmental deviations to adult psychopathological procrastination. Mol Psychiatry (2026). https://doi.org/10.1038/s41380-025-03423-0
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DOI: https://doi.org/10.1038/s41380-025-03423-0


