Abstract
Delay discounting (DD), the preference for smaller immediate over larger delayed rewards, is associated with impulsivity and cognitive control, representing a transdiagnostic process across different neuropsychiatric disorders. While previous neuroimaging studies have mainly focused on the functional neural substrates of DD, their anatomical correlates have received less attention. Based on accumulating evidence about the role of cortical sulci morphology as an indirect marker of fetal neurodevelopment, we examined the relationship between DD and the sulcal pattern of the anterior cingulate cortex (ACC), a cortical area classically associated with DD. In a large sample of young healthy adults (N = 390, 173 males), extracted from the Human Connectome Project (HCP) dataset, we defined the ACC sulcal pattern of each hemisphere as ‘single’ or ‘double parallel’ based on the absence or presence of the paracingulate sulcus (PCS), and then classified each individual brain as symmetric or asymmetric across the two hemispheres. DD rates were obtained from a Principal Component Analysis (PCA) of the results of a behavioral battery administered to the same participants. To ensure the specificity of the findings, statistical models were controlled for age, gender, and other cognitive factors, also derived from the PCA, as well as compared with the pattern of a different sulcus. Individuals with an asymmetric ACC sulcal pattern (i.e., inter-hemispheric differences in pattern type) exhibited lower discount rates, indicating a greater preference for delayed rewards, compared to those with a symmetric pattern. In the PCA-based analysis, the association significantly involved the factor capturing DD. Additional analysis on individual tasks supports this preferential relationship but further revealed an association between ACC morphology and processing speed. No comparable association was observed for the morphology of the Intra-Parietal Sulcus (IPS), used as a control region. Since sulcal patterns are determined during fetal life, our findings support a neurodevelopmental basis for individual differences in intertemporal choice and provide insights into the structural predisposition to impulsivity-related traits and their associated clinical pathologies. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00429-026-03114-8.