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Shared neurogenetic substrates of nonplanning impulsivity and procrastination.

Created on 08 Jul 2026

Authors

Yuanyuan Hu, Jie Xiang, Yuening Jin, Qingchen Fan, Changshuo Wang, Yihan Wu, Dang Zheng, Yancheng Tang, Wei Li, Bowen Hu, Tingyong Feng, Yuan Zhou, Zhiyi Chen

Published in

Proceedings of the National Academy of Sciences of the United States of America. Volume 123. Issue 28. Pages e2605127123. Jul 14, 2026. Epub Jul 07, 2026.

Abstract

Procrastination has a maladaptive impact on health and survival, yet it remains moderately heritable, presenting a biological paradox. Procrastination has been conceptualized as a byproduct of impulsivity, explaining its prevalence despite no discernible adaptive benefit. However, their shared neurobiological substrates have yet to be elucidated. Using a longitudinal twin cohort (N = 154), we show that nonplanning impulsivity (NPI) during late adolescence and early adulthood is prospectively associated with procrastination in later life. This effect was independently replicated in two cross-sectional cohorts (N = 327; N = 1,543). Twin modeling using an additive genetic and nonshared environmental (AE) framework, together with a meta-analysis of twin studies (N = 3,656 twin pairs), revealed significant shared genetic contributions (rg = 0.51). Beyond genetic overlap, neuroimaging meta-analysis (NeuroSynth meta-analysis for impulsivity: k = 198 studies, 5855 loci; mini meta-analysis for procrastination: k = 5 studies, 7 independent samples, Ncumulative = 893 participants), normative modeling (N = 37,407), and seed-based d mapping (SDM) converged on the left dorsolateral prefrontal cortex (DLPFC) as the region of maximal overlap between NPI and procrastination. The transcriptional profiles of the left DLPFC and impulsivity-associated genes exhibited functional convergence on regulation of biological and cellular processes. These genes showed brain-specific expression and associations with cortical metabolism, neurodegenerative disease, and developmental expression peaks, indicating a shared molecular basis for the neurogenetic architecture of procrastination. Together, our findings delineate a cross-scale characterization of the shared neurogenetic substrates linking NPI and procrastination, offering empirical evidence that elucidates the biological origins of procrastination.

PMID:
42412943
Bibliographic data and abstract were imported from PubMed on 08 Jul 2026.

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