Abnormal evidence accumulation underlies the positive memory deficit in depression.

Healthy adults show better memory for low-arousal positive versus negative stimuli, but depression compromises this positive memory advantage. Existing studies are limited by small samples or analyses that provide limited insight into underlying mechanisms. Our study addresses these concerns by using a multistaged analysis, including diffusion modeling, to identify precise psychological processes underlying the positive memory advantage and its disruption by depression in a large sample. A total of 1,358 participants completed the BDI-II (Beck et al., 1996) and an emotional memory task. At encoding, participants judged whether positive and negative words were positive or self-descriptive. After a free recall test, participants viewed an equal mix of studied and unstudied words and judged whether each was "old" or "new"; if judged "old," they indicated whether the study source was a valence or self-reference judgment. We replicate the positive memory advantage and its decrease in depression in recall, recognition, and source accuracy. The hierarchical drift diffusion model (HDDM; Wiecki et al., 2013) revealed that higher BDI-II scores are associated with more efficient evidence accumulation for negative words in the recognition and source memory tasks. By contrast, evidence accumulation for positive words is unaffected by BDI-II during the recognition task but becomes less efficient with increased BDI-II during the source memory task. In conclusion, in a well-controlled design with a large sample, we find that depression reduces the positive memory advantage. HDDM analyses suggest that this reflects differential effects of depression on the speed of evidence accumulation during the retrieval of positive versus negative memories. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Sluggish retrieval of positive memories in depressed adults.

Although depression is associated with poor memory for positive material, the underlying mechanisms remain unclear. We used the Hierarchical Drift Diffusion Model (HDDM) to determine whether slow evidence accumulation at retrieval contributes to depressed individuals' difficulty remembering positive events. Participants completed the Beck Depression Inventory-II and were stratified into High BDI (HBDI; BDI-II > 20, n = 49) and Low BDI (LBDI; BDI-II < 6, n = 46) groups. Next, participants completed an oddball task in which neutral, negative, and positive pictures served as rare targets. One day later, recognition memory was tested by presenting the encoded ("old") pictures along with closely matched ("new") lures. Recognition accuracy was analyzed with a generalized linear model, and choice and response time data were analyzed with the HDDM. Recognition accuracy for old positive pictures was lower in HBDI versus LBDI participants, and the HDDM highlighted slow evidence accumulation during positive memory retrieval in the HBDI group. Impaired memory for positive material in depressed adults was related to slow evidence accumulation at retrieval. Because oddballs should elicit prediction errors that normally strengthen memory formation, these retrieval findings may reflect weak positive prediction errors, at encoding, in depressed adults.

Forgiveness Mediates the Relationship Between Middle Frontal Gyrus Volume and Clinical Symptoms in Adolescents.

Dispositional forgiveness is positively associated with many facets of wellbeing and has protective implications against depression and anxiety in adolescents. However, little work has been done to examine neurobiological aspects of forgiveness as they relate to clinical symptoms. In order to better understand the neural mechanisms supporting the protective role of forgiveness in adolescents, the current study examined the middle frontal gyrus (MFG), which comprises the majority of the dorsolateral prefrontal cortex (DLPFC) and is associated with cognitive regulation, and its relationship to forgiveness and clinical symptoms in a sample of healthy adolescents. In this cross-sectional study (n = 64), larger MFG volume was significantly associated with higher self-reported dispositional forgiveness scores and lower levels of depressive and anxiety symptoms. Forgiveness mediated the relationship between MFG volume and both depressive and anxiety symptom levels. The mediating role of forgiveness in the relationship between MFG volume and clinical symptoms suggests that one way that cognitive regulation strategies supported by this brain region may improve adolescent mental health is via increasing a capacity for forgiveness. The present study highlights the relevance of forgiveness to neurobiology and their relevance to emotional health in adolescents. Future longitudinal studies should focus on the predictive quality of the relationship between forgiveness, brain volume and clinical symptoms and the effects of forgiveness interventions on these relationships.

Morphometric Biomarkers of Adolescents With Familial Risk for Alcohol Use Disorder.

BACKGROUND: While many adolescents exhibit risky behavior, teenagers with a family history (FH+) of an alcohol use disorder (AUD) are at a heightened risk for earlier initiation of alcohol use, a more rapid escalation in frequency and quantity of alcohol consumption and developing a subsequent AUD in comparison with youth without such family history (FH-). Neuroanatomically, developmentally normative risk-taking behavior parallels an imbalance between more protracted development of the prefrontal cortex (PFC) and earlier development of limbic regions. Magnetic resonance imaging (MRI)-derived volumetric properties were obtained for these structures in FH+ and FH- adolescents. METHODS: Forty-two substance-naïve adolescents (13- to 14-year-olds), stratified into FH+ (N = 19, 13 girls) and FH- (N = 23, 11 girls) age/handedness-matched groups, completed MRI scanning at 3.0T, as well as cognitive and clinical testing. T1 images were processed using FreeSurfer to measure PFC and hippocampi/amygdalae subfields/nuclei volumes. RESULTS: FH+ status was associated with larger hippocampal/amygdala volumes (p < 0.05), relative to FH- adolescents, with right amygdala results appearing to be driven by FH+ boys. Volumetric differences also were positively associated with family history density (p < 0.05) of having an AUD. Larger subfields/nuclei volumes were associated with higher anxiety levels and worse auditory verbal learning performance (p < 0.05). CONCLUSIONS: FH+ risk for AUD is detectable via neuromorphometric characteristics, which precede alcohol use onset and the potential onset of a later AUD, that are associated with emotional and cognitive measures. It is plausible that the development of limbic regions might be altered in FH+ youth, even prior to the onset of alcohol use, which could increase later risk. Thus, targeted preventative measures are warranted that serve to delay the onset of alcohol use in youth, particularly in those who are FH+ for an AUD.

A structural MRI study of differential neuromorphometric characteristics of binge and heavy drinking.

BACKGROUND: Alcohol misuse often manifests in two different patterns of drinking; Binge Drinking (BD; ≥4 (women) or ≥ 5 (men) drinks/day, ≤12 days/month) or Heavy Drinking (HD; ≥3 (women) or ≥4 (men) drinks/day, ≥16 days/month). Although direct comparisons have not been made, structural MRI studies indicate that the two types of drinking behaviors might be associated with different neuromorphometric characteristics. METHODS: This study used a cross-sectional design to compare brain structure (using MRI derived subcortical volume and cortical thickness measures) between participants with histories of BD (N = 16), HD (N = 15), and Healthy Controls (HC; N = 21). Whole-brain analyses were used to quantify group differences in subcortical volume and cortical thickness. Resulting cortical thickness clusters were quantified for their areas of overlap with resting-state network parcellations. RESULTS: BD was associated with decreased volumes of the bilateral global pallidus and decreased cortical thickness within the left superior-parietal cluster (p < .05). This cortical cluster overlapped in surface area with the dorsal-attention (50.86%) and the fronto-parietal network parcellations (49.14%). HD was associated with increased cortical thickness in the left medial occipito-parietal cluster (p < .05). This cluster primarily overlapped with the visual network parcellation (89%) and, to a lesser extent, with a widespread number of network parcellations (dorsal-attention: 3.8%; fronto-parietal: 3.5%; default-mode: 3.2%). CONCLUSIONS: These data indicate that histories of BD and HD patterns are associated with distinct neuromorphometric characteristics. BD was associated with changes within the executive control networks and the globus pallidus. HD was associated with widespread changes, that are primarily localized within the visual network.

Widespread effects of alcohol on white matter microstructure.

BACKGROUND: Evidence suggests that chronic misuse of alcohol may preferentially affect the integrity of frontal white matter (WM) tracts, which can impact executive functions important to achieve and maintain abstinence. METHODS: Global and regional WM microstructure was assessed using diffusion magnetic resonance measures of fractional anisotropy (FA) for 31 abstinent alcoholics (ALC) with an average of 25 years of abuse and approximately 5 years of sobriety and 20 nonalcoholic control (NC) participants. Data processing was conducted with FreeSurfer and FSL processing streams. Voxelwise processing of the FA data was carried out using tract-based spatial statistics. Clusters of significance were created to provide a quantitative summary of highly significant regions within the voxelwise analysis. RESULTS: Widespread, bilateral reductions in FA were observed in ALC as compared to NC participants in multiple frontal, temporal, parietal, and cerebellar WM tracts. FA in the left inferior frontal gyrus was associated with drinking severity. CONCLUSIONS: This study found widespread reductions in WM integrity in a group of ALC compared to NC participants, with most pronounced effects in frontal and superior tracts. Decreased FA throughout the frontostriatal circuits that mediate inhibitory control may result in impulsive behavior and inability to maintain sobriety.

White Matter and Cognitive Changes in Veterans Diagnosed with Alcoholism and PTSD.

Alcoholism frequently occurs in returning U.S. Veterans, and is often comorbid with Post Traumatic Stress Disorder (PTSD). The goal of this study was to investigate the relationship between white matter changes and neuropsychological alterations in Operation Enduring Freedom, and/or Operation Iraqi Freedom (OEF/OIF) alcoholic Veterans with two primary aims: (1) to examine the relationship of alcoholism to brain structure and function while controlling for the potential effects of comorbid PTSD, and (2) to examine whether the effects of alcoholism are moderated by the quantity of lifetime alcohol consumption. Our sample consisted of 71 deployed OEF/OIF Veterans stratified into four groups: alcoholics without PTSD, alcoholics with PTSD, participants with PTSD without comorbid alcoholism, and control participants without alcoholism or PTSD. Participants were given an extensive neuropsychological and psychiatric assessment battery, as well as Magnetic Resonance Diffusion Tensor Imaging (DT-MRI) scans. Results showed that disruption of executive functioning, and abnormal fractional anisotropy (FA; a measure of axonal integrity) within the frontal subcortical and dorsolateral frontal-parietal regions, occurred independently of the effects of PTSD. Furthermore, these cognitive and neuronal alterations were unique to the most severe subgroup of alcoholics who consumed the greatest amount of alcohol over the course of their lifetime, as compared to the rest of the sample. Axonal integrity within this subgroup, in regions underlying the frontal subcortical area, was shown to be decreased independently of cognitive changes. Integrity of axons underlying the dorsolateral frontal-parietal region, however, was increased. We hypothesized that this is a compensatory mechanism for executive dysfunction.

Effects of OEF/OIF-related physical and emotional co-morbidities on associative learning: concurrent delay and trace eyeblink classical conditioning.

This study examined the performance of veterans and active duty personnel who served in Operation Enduring Freedom and/or Operation Iraqi Freedom (OEF/OIF) on a basic associative learning task. Eighty-eight individuals participated in this study. All received a comprehensive clinical evaluation to determine the presence and severity of posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI). The eyeblink conditioning task was composed of randomly intermixed delay and trace conditioned stimulus (CS) and unconditioned stimulus (US) pairs (acquisition) followed by a series of CS only trials (extinction). Results revealed that those with a clinical diagnosis of PTSD or a diagnosis of PTSD with comorbid mTBI acquired delay and trace conditioned responses (CRs) to levels and at rates similar to a deployed control group, thus suggesting intact basic associative learning. Differential extinction impairment was observed in the two clinical groups. Acquisition of CRs for both delay and trace conditioning, as well as extinction of trace CRs, was associated with alcoholic behavior across all participants. These findings help characterize the learning and memory function of individuals with PTSD and mTBI from OEF/OIF and raise the alarming possibility that the use of alcohol in this group may lead to more significant cognitive dysfunction.

Reduced cortical thickness in abstinent alcoholics and association with alcoholic behavior.

BACKGROUND: Chronic misuse of alcohol results in widespread damage to the brain. Prior morphometric studies have examined cortical atrophy in individuals with alcoholism; however, no previous studies have examined alcohol-associated atrophy using cortical thickness measurements to obtain regional mapping of tissue loss across the full cortical surface. METHODS: We compared cortical thickness measures from 31 abstinent individuals with a history of prior alcohol abuse to 34 healthy nonalcoholic control participants (total sample size = 65). Cortical surface models were created from high-resolution T1-weighted images, and cortical thickness was then estimated as the distance between the gray matter/white matter boundary and the outer cortical surface. RESULTS: Abstinent alcoholics showed reduced whole-brain thickness as compared to nonalcoholic participants. Decreases in thickness were found bilaterally in (i) superior frontal, (ii) precentral, (iii) postcentral, (iv) middle frontal, (v) middle/superior temporal, (vi) middle temporal, and (vii) lateral occipital cortical regions. Decreased cortical thickness in the alcoholic group was associated with severity of alcohol abuse. CONCLUSIONS: These findings demonstrate widespread reduction in cortical thickness as a consequence of chronic alcoholism, with most severe reductions in frontal and temporal brain regions.

Silent trace eliminates differential eyeblink learning in abstinent alcoholics.

Chronic alcoholism has profound effects on the brain, including volume reductions in regions critical for eyeblink classical conditioning (EBCC). The current study challenged abstinent alcoholics using delay (n = 20) and trace (n = 17) discrimination/reversal EBCC. Comparisons revealed a significant difference between delay and trace conditioning performance during reversal (t (35) = 2.08, p < 0.05). The difference between the two tasks for discrimination was not significant (p = 0.44). These data support the notion that alcoholics are increasingly impaired in the complex task of reversing a previously learned discrimination when a silent trace interval is introduced. Alcoholics' impairment in flexibly altering learned associations may be central to their continued addiction.