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The BDNF val66met polymorphism (rs6265) influences activity-dependent secretion of brain-derived neurotrophic factor in the synapse, which is crucial for learning and memory. Individuals homozygous or heterozygous for the met allele have lower BDNF secretion than val homozygotes and may be at risk for reduced declarative memory performance, but it remains unclear which types of declarative memory may be affected and how aging of memory across the lifespan is impacted by the BDNF val66met polymorphism. This cross-sectional study investigated the effects of BDNF polymorphism on multiple indices of memory (item, associative, prospective, subjective complaints) in a lifespan sample of 116 healthy adults aged 20-93 years. Advancing age showed a negative effect on item, associative and prospective memory, but not on subjective memory complaints. For item and prospective memory, there were significant age x BDNF group interactions, indicating the adverse effect of age on memory performance across the lifespan was much stronger in the BDNF met carriers than for the val homozygotes. BDNF met carriers also endorsed significantly greater subjective memory complaints, regardless of age, and showed a trend (p < .07) toward poorer associative memory performance compared to val homozygotes. These results suggest that genetic predisposition to the availability of brain-derived neurotrophic factor, by way of the BDNF val66met polymorphism, exerts an influence on multiple indices of episodic memory – in some cases in all individuals regardless of age (subjective memory and perhaps associative memory), in others as an exacerbation of age-related differences in memory across the lifespan (item and prospective memory).

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Objective: Distress tolerance (DT), the ability to withstand aversive internal states, represents an important risk factor for substance use relapse and a potential treatment target. Neurobiological research in substance using populations suggests that continued substance use could erode DT, whereas abstinence could bolster it. The current study characterized trajectories of behavioral and self-reported indices of DT and examined the prospective effect of substance use on DT trajectories among those seeking treatment for substance use. Method: Individuals (N = 263, Mage = 42.68, SD = 11.8, 70.7% male, 94.7% African American) in residential substance use treatment completed subjective (Distress Tolerance Scale) and behavioral (Mirror Tracing Persistence Task–computerized version) DT measures, as well as report of daily substance use (timeline follow-back) over 5 assessment time-points from pretreatment to 12 months posttreatment. Latent curve modeling estimated DT trajectories and their associations with substance use behavior, including abstinence duration (days until first use) and substance use frequency (percentage of substance use days between assessments). Results: Self-reported and behavioral DT indicators both exhibited positive, nonlinear change over time (standardized slope parameter estimates: Distress Tolerance Scale β = 0.61, p < .01; Mirror Tracing Persistence Task β = 0.34, p < .01). Abstinence duration was associated with greater improvement in behavioral (β = .20, p = .03) DT specifically. Frequency of use was statistically significantly associated with attenuated behavioral DT at 6-month (β = −.12, p = .03) and 12-month follow-ups (β = −.08, p = .045). Conclusions: DT appears to improve appreciably posttreatment, and return to substance use may shape the degree of this improvement. Collectively, these findings support the conceptualization of DT as a malleable treatment target and emphasize the benefit of abstinence on improvement in DT.

Distress tolerance (DT), a predictor of substance use treatment retention and post-treatment relapse, is associated with task based neural activation in regions located within the salience (SN), default mode (DMN), and executive control networks (ECN). The impact of network connectivity on DT has yet to be investigated. The aim of the present study was to test within and between network resting-state functional connectivity (rsFC) associations with DT, and the impact of cocaine use on this relationship. Twenty-nine adults reporting regular cocaine use (CU) and 28 matched healthy control individuals (HC), underwent resting-state functional magnetic resonance imaging followed by the completion of two counterbalanced, computerized DT tasks. Dual-regression analysis was used to derive within and between network rsFC of the SN, DMN, and lateralized (left and right) ECN. Cox proportional-hazards survival models were used to test the interactive effect of rsFC and group on DT. The association between cocaine use severity, rsFC, and DT was tested within the CU group. Lower LECN and higher DMN-SN rsFC were associated with DT impairment. Greater amount of cocaine use per using day was associated with greater DMN-SN rsFC. The findings emphasize the role of neural resource allocation within the ECN and between DMN-SN on distress tolerance.