Objective
Cognitive reserve (CR) refers to the brain’s capacity to cope with pathology and preserve functioning. We investigated cognitive performance between individuals with alcohol use disorder (AUD) and healthy controls to examine whether CR, operationalized as education and psychosocial functioning, influences neuropsychological functioning.
Method
We recruited 45 AUD (DSM-V criteria) who reported drinking levels exceeding NIAAA guidelines (>14/7 drinks/week for men/women) and 30 healthy controls who did not. MANCOVAs controlling for CR were used to investigate between-group differences in neuropsychological performance, as measured by the NIH Toolbox. A series of linear regression analyses were also performed to evaluate effects of AUD and CR on neuropsychological performance. Psychosocial functioning, education, and AUD status were simultaneously entered as predictors of Flanker, Dimensional Change Card Sort, Picture Sequence, List Sort, and Processing Speed scores.
Results
MANCOVAs revealed a significantly slower processing speed in the AUD group compared to controls when controlling for CR (F = 4.30, p = .042). There were no significant group differences on other tests. Linear regressions showed only processing speed to be predicted by AUD (β = −.255, p = .042), while CR measures were not. Education predicted Picture Sequence (β = .245, p = .041) and Card Sort (β = .291, p = .009) performance, and psychosocial functioning predicted Flanker (β = .296, p = .021) and Card Sort (β = .316, p = .010) performance.
Conclusions
CR appears to contribute to higher-order cognitive functions, regardless of AUD status. Only processing speed, a domain typically susceptible to brain pathology, was significantly related to AUD. Thus, factors linked to CR may serve as important targets for future research and intervention in AUD to promote favorable cognitive outcomes.
Large proportions of smokers are unsuccessful in evidence-based smoking cessation treatment and identifying prognostic predictors may inform improvements in treatment. Steep discounting of delayed rewards (delay discounting) is a robust predictor of poor smoking cessation outcome, but the underlying neural predictors have not been investigated. Forty-one treatment-seeking adult smokers completed a functional magnetic resonance imaging (fMRI) delay discounting paradigm prior to initiating a 9-week smoking cessation treatment protocol. Behavioral performance significantly predicted treatment outcomes (verified 7-day abstinence, n = 18; relapse, n = 23). Participants in the relapse group exhibited smaller area under the curve (d = 1.10) and smaller AUC was correlated with fewer days to smoking relapse (r = .56, p<.001) Neural correlates of discounting included medial and dorsolateral prefrontal cortex, posterior cingulate, precuneus, and anterior insula, and interactions between choice type and relapse status were present for the dorsolateral prefrontal cortex, precuneus, and the striatum. This initial investigation implicates differential neural activity in regions associated with frontal executive and default mode activity, as well as motivational circuits. Larger samples are needed to improve the resolution in identifying the neural underpinnings linking steep delay discounting to smoking cessation.
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