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Hendershot C.S.,Campbell Family Mental Health Research Institute | Hendershot C.S.,University of Toronto | Claus E.D.,Lovelace Biomedical and Environmental Research Institute | Ramchandani V.A.,U.S. National Institutes of Health
Addiction Biology

Human laboratory and animal models implicate variation in the μ-opioid receptor gene (OPRM1) as relevant for alcohol-related reward. OPRM1 is associated with alcohol self-administration in non-human primate studies, but the relevance of this finding to human models is unclear. This study used computer-assisted self-infusion of ethanol (CASE) to examine associations among OPRM1 A118G genotype, subjective responses to alcohol and intravenous alcohol self-administration in young heavy drinkers (n = 40, mean age = 19.95 years, SD = 0.82). Participants completed a 2-hour CASE session comprising a priming phase followed by ad libitum self-administration in a free-access paradigm. Participants achieved a mean peak breath alcohol concentration (BrAC) of 81.18 mg% (SD = 24.96). Those with the OPRM1 118G variant (GA or GG genotypes) achieved significantly higher peak BrAC (M = 94.90 mg%, SD = 16.56) than those with the AA genotype (M = 74.46 mg%, SD = 25.36), reflecting a significantly greater number of alcohol requests among GA/GG participants. Eighty percent of GA/GG participants surpassed a threshold defining a laboratory analog of heavy alcohol exposure (80 mg%) compared with 46 percent of AA participants. Results indicated significant associations between subjective measures of alcohol sensitivity and CASE outcomes, although the pattern of findings differed across self-report measures. Subjective responses did not differ by OPRM1 status. These results offer further support for the feasibility of the CASE paradigm and provide initial evidence for an association of OPRM1 with alcohol self-administration in a human laboratory context. © 2014 Society for the Study of Addiction. Source

Calhoun V.D.,Lovelace Biomedical and Environmental Research Institute | Calhoun V.D.,University of New Mexico | Sui J.,Lovelace Biomedical and Environmental Research Institute | Sui J.,Brainnetome Center | Sui J.,CAS Institute of Automation
Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

It is becoming increasingly clear that combining multimodal brain imaging data provides more information for individual subjects by exploiting the rich multimodal information that exists. However, the number of studies that do true multimodal fusion (i.e., capitalizing on joint information among modalities) is still remarkably small given the known benefits. In part, this is because multimodal studies require broader expertise in collecting, analyzing, and interpreting the results than do unimodal studies. In this article, we start by introducing the basic reasons why multimodal data fusion is important and what it can do and, importantly, how it can help us avoid wrong conclusions and help compensate for imperfect brain imaging studies. We also discuss the challenges that need to be confronted for such approaches to be more widely applied by the community. We then provide a review of the diverse studies that have used multimodal data fusion (primarily focused on psychosis) as well as provide an introduction to some of the existing analytic approaches. Finally, we discuss some up-and-coming approaches to multimodal fusion including deep learning and multimodal classification that show considerable promise. Our conclusion is that multimodal data fusion is rapidly growing, but it is still underutilized. The complexity of the human brain coupled with the incomplete measurement provided by existing imaging technology makes multimodal fusion essential to mitigate misdirection and hopefully provide a key to finding the missing link(s) in complex mental illness. © 2016 Society of Biological Psychiatry. Source

Anderson N.E.,Lovelace Biomedical and Environmental Research Institute | Anderson N.E.,University of New Mexico | Kiehl K.A.,Lovelace Biomedical and Environmental Research Institute | Kiehl K.A.,University of New Mexico
Restorative Neurology and Neuroscience

Psychopathy is a mental disorder marked by deficient emotional responses, lack of empathy, and poor behavioral controls, commonly resulting in persistent antisocial deviance and criminal behavior. Accumulating research suggests that psychopathy follows a developmental trajectory with strong genetic influences, and which precipitates deleterious effects on widespread functional networks, particularly within paralimbic regions of the brain. While traditional therapeutic interventions commonly administered in prisons and forensic institutions have been notoriously ineffective at combating these outcomes, alternative strategies informed by an understanding of these specific neuropsychological obstacles to healthy development, and which target younger individuals with nascent symptoms of psychopathy are more promising. Here we review recent neurobehavioral and neuroimaging literature that informs our understanding of the brain systems compromised in psychopathy, and apply these data to a broader understanding of its developmental course, ultimately promoting more proactive intervention strategies profiting from adaptive neuroplasticity in youth. © 2014 - IOS Press and the authors. All rights reserved. Source

Dodd A.B.,Lovelace Biomedical and Environmental Research Institute | Epstein K.,Lovelace Biomedical and Environmental Research Institute | Ling J.M.,Lovelace Biomedical and Environmental Research Institute | Mayer A.R.,Lovelace Biomedical and Environmental Research Institute | Mayer A.R.,University of New Mexico
Journal of Neurotrauma

The past 10 years have seen a rapid increase in the use of diffusion tensor imaging to identify biomarkers of traumatic brain injury (TBI). Although the literature generally indicates decreased anisotropic diffusion at more chronic injury periods and in more severe injuries, considerable debate remains regarding the direction (i.e., increased or decreased) of anisotropic diffusion in the acute to semi-acute phase (here defined as less than 3 months post-injury) of mild TBI (mTBI). A systematic review of the literature was therefore performed to (1) determine the prevalence of different anisotropic diffusion findings (increased, decreased, bidirectional, or null) during the semi-acute injury phase of mTBI and to (2) identify clinical (e.g., age of injury, post-injury scan time, etc.) and experimental factors (e.g., number of unique directions, field strength) that may influence these findings. Results from the literature review indicated 31 articles with independent samples of semi-acute mTBI patients, with 13 studies reporting decreased anisotropic diffusion, 11 reporting increased diffusion, 2 reporting bidirectional findings, and 5 reporting null findings. Chi-squared analyses indicated that the total number of diffusion-weighted (DW) images was significantly associated with findings of either increased (DW≥30) versus decreased (DW≤25) anisotropic diffusion. Other clinical and experimental factors were not statistically significant for direction of anisotropic diffusion, but these results may have been limited by the relatively small number of studies within each domain (e.g., pediatric studies). In summary, current results indicate roughly equivalent number of studies reporting increased versus decreased anisotropic diffusion during semi-acute mTBI, with the number of unique diffusion images being statistically associated with the direction of findings. © Copyright 2014, Mary Ann Liebert, Inc. Source

Ling J.M.,Lovelace Biomedical and Environmental Research Institute | Klimaj S.,Lovelace Biomedical and Environmental Research Institute | Toulouse T.,Lovelace Biomedical and Environmental Research Institute | Mayer A.R.,Lovelace Biomedical and Environmental Research Institute | Mayer A.R.,University of New Mexico

Objective: To examine the underlying pathophysiology of mild traumatic brain injury through changes in gray matter diffusion and atrophy during the semiacute stage. Methods: Fifty patients and 50 sex-, age-, and education-matched controls were evaluated with a clinical and neuroimaging battery approximately 14 days postinjury, with 26 patients returning for follow-up 4 months postinjury. Clinical measures included tests of attention, processing speed, executive function, working memory, memory, and self-reported postconcussive symptoms. Measures of diffusion (fractional anisotropy [FA], mean diffusivity) and atrophy were obtained for cortical and subcortical structures to characterize effects of injury as a function of time. Results: Patients reported more cognitive, somatic, and emotional complaints during the semiacute injury phase, which were significantly reduced 4 months postinjury. Patients showed evidence of increased FA in the bilateral superior frontal cortex during the semiacute phase, with the left superior frontal cortex remaining elevated 4 months postinjury. There were no significant differences between patients and matched controls on neuropsychological testing or measures of gray matter atrophy/mean diffusivity at either time point. Conclusions: Increased cortical FA is largely consistent with an emerging animal literature of gray matter abnormalities after neuronal injury. Potential mechanistic explanations for increased FA include cytotoxic edema or reactive gliosis. In contrast, there was no evidence of cortical or subcortical atrophy in the current study, suggesting that frank neuronal or neuropil loss does not occur early in the chronic disease course for patients with typical mild traumatic brain injury. © 2013 American Academy of Neurology. Source

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