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Moeller, F. G.

Publications and source records attributed to Moeller, F. G..

2 recordsLinked to original sources
bioRxiv2018

Neurocognitive and psychiatric markers for addiction: Common vs. specific (endo)phenotypes for opiate and stimulant dependence

BACKGROUNDThe differential utility of neurocognitive impulsivity and externalizing/internalizing traits as putative addiction endophenotypes among individuals dependent on opiates vs. stimulants is unclear. The present study aims to determine: (1) whether neurocognitive impulsivity dimensions and externalizing/internalizing traits are correlated between siblings discordant for opiate and stimulant dependence; and (2) which of these associations are common across substances and which are substance-specific.\n\nMETHODPearson correlations between individuals with pure heroin and pure amphetamine dependence and their unaffected biological siblings (n = 37 heroin sibling pairs; n = 30 amphetamine sibling pairs) were run on 10 neurocognitive measures, 6 externalizing measures, and 5 internalizing measures. Sibling pair effects were further examined using regression.\n\nRESULTSSiblings discordant for heroin dependence were significantly correlated on delay aversion on the Cambridge Gambling Task, risk-taking on the Balloon Analogue Risk Task, sensation seeking, and hopelessness. Siblings discordant for amphetamine dependence were significantly correlated on quality of decision-making on the Cambridge Gambling Task, discriminability on the Immediate Memory Task, commission errors on the Go/No-Go Task, trait impulsivity, ADHD, and anxiety sensitivity.\n\nCONCLUSIONSDimensions of impulsivity and externalizing/internalizing traits appear to aggregate among siblings discordant for substance dependence. Risk-taking propensity, sensation seeking, and hopelessness were specific for heroin sibling pairs. Motor/action impulsivity and trait impulsivity were specific to amphetamine sibling pairs. Decisional/choice impulsivity was common across both heroin and amphetamine sibling pairs. These findings provide preliminary evidence for the utility of neurocognitive impulsivity and externalizing/internalizing traits as candidate endophenotypes for substance dependence in general and for substance-specific dependencies.

neuroscience↗
bioRxiv2018

Measures of Possible Allostatic Load in Comorbid Cocaine and Alcohol use Disorder: Brain White Matter Integrity, Telomere Length, and Anti-Saccade Performance

Chronic cocaine and alcohol use impart significant stress on biological and cognitive systems, resulting in changes consistent with an allostatic load model of neurocognitive impairment. The present study measured potential markers of allostatic load in individuals with comorbid cocaine/alcohol use disorders (CUD/AUD) and control subjects. Measures of brain white matter (WM) integrity, telomere length, and impulsivity/attentional bias were obtained. WM integrity (CUD/AUD only) was indexed by diffusion tensor imaging metrics, including radial diffusivity (RD) and fractional anisotropy (FA). Telomere length was indexed by T/S ratio. Impulsivity and attentional bias to drug cues were measured via eye-tracking, and were also modeled using the Hierarchical Diffusion Drift Model (HDDM). Average whole-brain RD and FA were associated with years of cocaine use (R2 = 0.56 and 0.51, both p < .005) but not years of alcohol use. CUD/AUD subjects showed more anti-saccade errors (p < .01), greater attentional bias scores (p < .001), and higher HDDM drift rates on cocaine-cue trials (Bayesian probability CUD/AUD > control = p > 0.99). Telomere length was shorter in CUD/AUD, but the difference was not statistically significant. Within the CUD/AUD group, exploratory regression using an elastic-net model determined that more years of cocaine use, older age, larger HDDM drift rate differences and shorter telomere length were all predictive of white matter integrity as measured by RD (model R2 = 0.79). Collectively, the results provide modest support linking CUD/AUD to putative markers of allostatic load.

neuroscience↗