RT Journal Article
SR Electronic
T1 Evidence accumulation and associated error-related brain activity as computationally informed prospective predictors of substance use in emerging adulthood
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.03.06.981035
DO 10.1101/2020.03.06.981035
A1 Alexander S. Weigard
A1 Sarah J. Brislin
A1 Lora M. Cope
A1 Jillian E. Hardee
A1 Meghan E. Martz
A1 Alexander Ly
A1 Robert A. Zucker
A1 Chandra Sripada
A1 Mary M. Heitzeg
YR 2020
UL http://biorxiv.org/content/early/2020/03/08/2020.03.06.981035.abstract
AB Substance use peaks during the developmental period known as emerging adulthood (roughly ages 18–25), but not every individual who uses substances during this period engages in frequent or problematic use. Previous studies have suggested that individual differences in neurocognition may prospectively predict problematic substance use, but mechanistic neurocognitive risk factors with clear links to both behavior and neural circuitry have not yet been identified. Here we take an approach rooted in computational psychiatry, an emerging field in which formal models of neurocognition are used to identify candidate biobehavioral dimensions that confer risk for psychopathology. Specifically, we test whether lower efficiency of evidence accumulation (EEA), a computationally tractable process that drives neurocognitive performance across many tasks, is a risk factor for substance use in emerging adults. In an fMRI substudy within a sociobehavioral longitudinal study (n=106), we find that lower EEA and reductions in a robust neural-level correlate of EEA (error-related activations in salience network and parietal structures) measured at ages 18–21 are both prospectively related to higher levels of substance use during ages 22–26, even after adjusting for other well-known risk factors. Results from Bayesian model comparisons corroborated inferences from conventional hypothesis testing and provided evidence that both EEA and its neural correlates contain unique predictive information about substance use involvement. Overall, these findings suggest that EEA is a mechanistic, computationally tractable neurocognitive risk factor for substance use at a critical developmental period, with clear links to both neural correlates and well-established formal theories of brain function.