The origins of cognitive flexibility in chimpanzees.

Cognitive flexibility is a core component of executive function, a suite of cognitive capacities that enables individuals to update their behavior in dynamic environments. Human executive functions are proposed to be enhanced compared to other species, but this inference is based primarily on neuroanatomical studies. To address this, we examined the nature and origins of cognitive flexibility in chimpanzees, our closest living relatives. Across three studies, we examined different components of cognitive flexibility using reversal learning tasks where individuals first learned one contingency and then had to shift responses when contingencies flipped. In Study 1, we tested n = 82 chimpanzees ranging from juvenility to adulthood on a spatial reversal task, to characterize the development of basic shifting skills. In Study 2, we tested how n = 24 chimpanzees use spatial versus arbitrary perceptual information to shift, a proposed difference between human and nonhuman cognition. In Study 3, we tested n = 40 chimpanzees on a probabilistic reversal task. We found an extended developmental trajectory for basic shifting and shifting in response to probabilistic feedback-chimpanzees did not reach mature performance until late in ontogeny. Additionally, females were faster to shift than males were. We also found that chimpanzees were much more successful when using spatial versus perceptual cues, and highly perseverative when faced with probabilistic versus consistent outcomes. These results identify both core features of chimpanzee cognitive flexibility that are shared with humans, as well as constraints on chimpanzee cognitive flexibility that may represent evolutionary changes in human cognitive development.

Psychopathic individuals exhibit but do not avoid regret during counterfactual decision making.

Psychopathy is associated with persistent antisocial behavior and a striking lack of regret for the consequences of that behavior. Although explanatory models for psychopathy have largely focused on deficits in affective responsiveness, recent work indicates that aberrant value-based decision making may also play a role. On that basis, some have suggested that psychopathic individuals may be unable to effectively use prospective simulations to update action value estimates during cost-benefit decision making. However, the specific mechanisms linking valuation, affective deficits, and maladaptive decision making in psychopathy remain unclear. Using a counterfactual decision-making paradigm, we found that individuals who scored high on a measure of psychopathy were as or more likely than individuals low on psychopathy to report negative affect in response to regret-inducing counterfactual outcomes. However, despite exhibiting intact affective regret sensitivity, they did not use prospective regret signals to guide choice behavior. In turn, diminished behavioral regret sensitivity predicted a higher number of prior incarcerations, and moderated the relationship between psychopathy and incarceration history. These findings raise the possibility that maladaptive decision making in psychopathic individuals is not a consequence of their inability to generate or experience negative emotions. Rather, antisocial behavior in psychopathy may be driven by a deficit in the generation of forward models that integrate information about rules, costs, and goals with stimulus value representations to promote adaptive behavior.

Chimpanzee Cooperation Is Fast and Independent From Self-Control.

Large-scale cooperation is a hallmark of our species and appears to be unique among primates. Yet the evolutionary mechanisms that drove the emergence of humanlike patterns of cooperation remain unclear. Studying the cognitive processes underlying cooperative behavior in apes, our closest living relatives, can help identify these mechanisms. Accordingly, we employed a novel test battery to assess the willingness of 40 chimpanzees to donate resources, instrumentally help others, and punish a culpable thief. We found that chimpanzees were faster to make prosocial than selfish choices and that more prosocial individuals made the fastest responses. Further, two measures of self-control did not predict variation in prosocial responding, and individual performance across cooperative tasks did not covary. These results show that chimpanzees and humans share key cognitive processes for cooperation, despite differences in the scope of their cooperative behaviors.

Dopaminergic mechanisms of individual differences in human effort-based decision-making.

Preferences for different combinations of costs and benefits are a key source of variability in economic decision-making. However, the neurochemical basis of individual differences in these preferences is poorly understood. Studies in both animals and humans have demonstrated that direct manipulation of the neurotransmitter dopamine (DA) significantly impacts cost/benefit decision-making, but less is known about how naturally occurring variation in DA systems may relate to individual differences in economic behavior. In the present study, 25 healthy volunteers completed a dual-scan PET imaging protocol with [(18)F]fallypride and d-amphetamine to measure DA responsivity and separately completed the effort expenditure for rewards task, a behavioral measure of cost/benefit decision-making in humans. We found that individual differences in DA function in the left striatum and ventromedial prefrontal cortex were correlated with a willingness to expend greater effort for larger rewards, particularly when probability of reward receipt was low. Additionally, variability in DA responses in the bilateral insula was negatively correlated with willingness to expend effort for rewards, consistent with evidence implicating this region in the processing of response costs. These findings highlight the role of DA signaling in striatal, prefrontal, and insular regions as key neurochemical mechanisms underlying individual differences in cost/benefit decision-making.

Distinct developmental trajectories for risky and impulsive decision-making in chimpanzees.

Human adolescence is characterized by a suite of changes in decision-making and emotional regulation that promote risky and impulsive behavior. Accumulating evidence suggests that behavioral and physiological shifts seen in human adolescence are shared by some primates, yet it is unclear if the same cognitive mechanisms are recruited. We examined developmental changes in risky choice, intertemporal choice, and emotional responses to decision outcomes in chimpanzees, our closest-living relatives. We found that adolescent chimpanzees were more risk-seeking than adults, as in humans. However, chimpanzees showed no developmental change in intertemporal choice, unlike humans, although younger chimpanzees did exhibit elevated emotional reactivity to waiting compared to adults. Comparisons of cortisol and testosterone indicated robust age-related variation in these biomarkers, and patterns of individual differences in choices, emotional reactivity, and hormones also supported a developmental dissociation between risk and choice impulsivity. These results show that some but not all core features of human adolescent decision-making are shared with chimpanzees. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Examining tradeoffs between cognitive effort and relief among adults with self-injurious behavior.

BACKGROUND: People engage in nonsuicidal self-injury (NSSI) to reduce negative affect, but it is not clear why they engage in this harmful type of behavior instead of using healthier strategies. The primary goal of this study was to evaluate whether people choose NSSI to reduce negative affect because they perceive it to be less cognitively costly than other available strategies. METHOD: In experiment one, 43 adults completed a novel, relief-based effort discounting task designed to index preferences about exerting cognitive effort to achieve relief. In experiment two, 149 adults, 52 % with a history of NSSI, completed our effort discounting task. RESULTS: Our main results suggest that people will accept less relief from an aversive experience if doing so requires expending less effort, i.e. they demonstrate effort discounting in the context of decisions about relief. We also found and that effort discounting is stronger among those with a history of NSSI, but this association became nonsignificant when simultaneously accounting for other conditions associated with aberrant effort tradeoffs. LIMITATIONS: The use of a control group without NSSI or other potentially harmful relief-seeking behaviors limits our ability to draw specific conclusions about NSSI. The ecological validity of our task was limited by a modestly effective affect manipulation, and because participants made hypothetical choices. CONCLUSIONS: This study demonstrates that preferences about exerting cognitive effort may be a barrier to using healthier affect regulation strategies. Further, the preference not to exert cognitive effort, though present in NSSI, is likely not unique to NSSI. Instead, effort discounting may be a transdiagnostic mechanism promoting an array of harmful relief-seeking behaviors.

The association of impulsivity with effects of the ChooseWell 365 workplace nudge intervention on diet and weight.

Impulsivity is associated with unhealthy food choices. Nudge interventions in the food environment may be particularly helpful for individuals with high impulsivity. To examine if trait, choice, and action impulsivity were associated with the effectiveness of a workplace-based nudge intervention to improve diet and weight. This was a planned secondary analysis of 487 participants of ChooseWell 365, a randomized controlled trial that tested a 12-month nudge intervention to improve cafeteria purchases among hospital employees. Trait impulsivity was measured with the Barratt Impulsiveness Scale. Choice and action impulsivity were assessed with delay discounting and response inhibition tasks, respectively. Tertiles were generated for each measure. Multivariable regression models examined the association of impulsivity with cafeteria purchases [Healthy Purchasing Score (HPS)] over 12 months, dietary intake [Healthy Eating Index-2015 (HEI) score], and body mass index (BMI) measured at 12 months. Interaction terms tested differences in intervention effect by level of impulsivity. Participants with higher trait (p = .02) and choice (p < .001) impulsivity had lower baseline HPS than those with lower impulsivity. Employees of all impulsivity levels increased healthy eating, but higher trait impulsivity was associated with smaller increase in HPS over 12 months (p = .03). In the highest action impulsivity tertile, 12-month BMI increased less for intervention vs. control participants (0.3 vs. 0.5 kg/m2; p-interaction = .04). There were no interaction effects for trait or choice impulsivity. A workplace nudge intervention improved food choices among employees of all impulsivity levels and attenuated weight gain in those with higher action impulsivity.

Impulsivity is an individual trait characterized by the tendency to make quick or rash decisions. High impulsivity is associated with less healthy food choices and poorer health outcomes, including obesity. "Nudges", which are small interventions that steer people towards healthy choices without removing other options, may be particularly helpful for individuals with high impulsivity. Our study tested whether trait impulsivity (i.e., impulsive personality tendencies), choice impulsivity (i.e., preference for immediate vs. later rewards), and action impulsivity (i.e., low behavioral inhibition) were associated with the effectiveness of a workplace nudge intervention to increase healthy food choices and slow weight gain among hospital employees. We found that higher trait and choice impulsivity were associated with less healthy food purchases in the study population at baseline, but employees of all levels of impulsivity improved their food purchases in response to the intervention. The intervention may have helped slow weight gain in individuals with high action impulsivity.

Characterizing mood disorders in the AFFECT study: a large, longitudinal, and phenotypically rich genetic cohort in the US.

There has recently been marked progress in identifying genetic risk factors for major depression (MD) and bipolar disorder (BD); however, few systematic efforts have been made to elucidate heterogeneity that exists within and across these diagnostic taxa. The Affective disorders, Environment, and Cognitive Trait (AFFECT) study presents an opportunity to identify and associate the structure of cognition and symptom-level domains across the mood disorder spectrum in a prospective study from a diverse US population.Participants were recruited from the 23andMe, Inc research participant database and through social media; self-reported diagnosis of MD or BD by a medical professional and medication status data were used to enrich for mood-disorder cases. Remote assessments were used to acquire an extensive range of phenotypes, including mood state, transdiagnostic symptom severity, task-based measures of cognition, environmental exposures, personality traits. In this paper we describe the study design, and the demographic and clinical characteristics of the cohort. In addition we report genetic ancestry, SNP heritability, and genetic correlations with other large cohorts of mood disorders.A total of 48,467 participants were enrolled: 14,768 with MD, 9864 with BD, and 23,835 controls. Upon enrollment, 47% of participants with MD and 27% with BD indicated being in an active mood episode. Cases reported early ages of onset (mean = 13.2 and 14.3 years for MD and BD, respectively), and high levels of recurrence (78.6% and 84.9% with >5 episodes), psychotherapy, and psychotropic medication use. SNP heritability on the liability scale for the ascertained MD participants (0.19-0.21) was consistent with the high level of disease severity in this cohort, while BD heritability estimates (0.16-0.22) were comparable to reports in other large scale genomic studies of mood disorders. Genetic correlations between the AFFECT cohort and other large-scale cohorts were high for MD but not for BD. By incorporating transdiagnostic symptom assessments, repeated measures, and genomic data, the AFFECT study represents a unique resource for dissecting the structure of mood disorders across multiple levels of analysis. In addition, the fully remote nature of the study provides valuable insights for future virtual and decentralized clinical trials within mood disorders.

A unique role for the human amygdala in novelty detection.

Previous research indicates that the amygdala and hippocampus are sensitive to novelty; however, two types of novelty can be distinguished - stimuli that are ordinary, but novel in the current context, and stimuli that are unusual. Using functional magnetic resonance imaging, we examined blood oxygen dependent level (BOLD) response of the human amygdala and hippocampus to novel, commonly seen objects versus novel unusual objects. When presented with the novel common stimuli, the BOLD signal increased significantly in both the amygdala and hippocampus. However, for the novel unusual stimuli, only the amygdala showed an increased response compared to the novel common stimuli. These findings suggest that the amygdala is distinctly responsive to novel unusual stimuli, making a unique contribution to the novelty detection circuit.

MAOA and the neurogenetic architecture of human aggression.

Antisocial aggression is a widespread and expensive social problem. Although aggressive behaviors and temperament are highly heritable, clinical and trait associations for the most promising candidate gene for aggression, MAOA, have been largely inconsistent. We suggest that limitations inherent to that approach might be overcome by using multimodal neuroimaging to characterize neural mechanisms of genetic risk. Herein, we detail functional, structural and connectivity findings implicating the low-expressing allele of the MAOA u-VNTR (MAOA-L) in adversely prejudicing information processing within a corticolimbic circuit composed of amygdala, rostral cingulate and medial prefrontal cortex. We propose that the MAOA-L, by causing an ontogenic excess of 5-hydroxytryptamine, labilizes critical neural circuitry for social evaluation and emotion regulation (the 'socioaffective scaffold'), thereby amplifying the effects of adverse early-life experience and creating deleterious sociocognitive biases. Our construct provides a neurobiologically consistent model for gene-environment interactions in impulsive aggression.

Are suicide attempters more impulsive than suicide ideators?

OBJECTIVE: For over 100 years impulsiveness has been cited as a key factor in why some people that think about killing themselves go on to attempt suicide. Yet prior studies are limited by not using experimental groups that can test this hypothesis and by treating impulsiveness as a unidimensional construct. To overcome these limitations, we compared suicide ideators and suicide attempters on several dimensions of impulsiveness. METHOD: In Study 1 we compared inpatient suicide attempters who made an attempt within the prior two weeks (n = 30), current inpatient suicide ideators (n = 31), and community controls (n = 34) on several dimensions of impulsiveness using self-report and behavioral measures. In Study 2 (n = 346), we compared three similar groups based on lifetime and past year suicidal behaviors on several of the measures in Study 1. RESULTS: In Study 1, we found only that negative urgency was clearly elevated among attempters compared with ideators. In Study 2, there were no significant differences on any impulsiveness constructs, including negative urgency. CONCLUSIONS: Results from the two studies suggest that attempters may not have significantly elevated trait impulsiveness, compared to ideators; however, attempters may have higher impulsiveness when in a negative state.

Allelic variation in RGS4 impacts functional and structural connectivity in the human brain.

Regulator of G-protein signaling 4 (RGS4) modulates postsynaptic signal transduction by affecting the kinetics of G alpha-GTP binding. Linkage, association, and postmortem studies have implicated the gene encoding RGS4 (RGS4) as a schizophrenia susceptibility factor. Using a multimodal neuroimaging approach, we demonstrate that genetic variation in RGS4 is associated with functional activation and connectivity during working memory in the absence of overt behavioral differences, with regional gray and white matter volume and with gray matter structural connectivity in healthy human subjects. Specifically, variation at one RGS4 single nucleotide polymorphism that has been associated previously with psychosis (rs951436) impacts frontoparietal and frontotemporal blood oxygenation level-dependent response and network coupling during working memory and results in regionally specific reductions in gray and white matter structural volume in individuals carrying the A allele. These findings suggest mechanisms in brain for the association of RGS4 with risk for psychiatric illness.

COMT genetic variation affects fear processing: psychophysiological evidence.

Emotional dysregulation is a core characteristic of many psychiatric diseases, including the anxiety disorders. Although heritable influences account for a significant degree of variation in risk for such disorders, relatively few candidate susceptibility factors have been identified. A coding variant in one such gene, encoding the dopamine catabolic enzyme catechol-O-methyltransferase (COMT Val158Met), has previously been associated with anxiety and with anxiety-related temperament and altered neural responses to affective stimuli in healthy individuals. In 96 healthy women recruited from a sample of 800 participants according to genotype, the authors tested for an association between the DRD2/ANKK1 Taq Ia, the COMT Val158Met, and a psychophysiological measure of emotion processing, the acoustic affective startle reflex modulation (ASRM) paradigm, and found that COMT genotype significantly affected startle reflex modulation by aversive stimuli, with Met158 homozygotes exhibiting a markedly potentiated startle reflex compared with Val158 carriers. A trait measure of anxiety (Gray's Behavioral Inhibition System; J. A. Gray & N. McNaughton, 2000) was also associated with ASRM. The functional polymorphism in the dopamine D2 receptor (DRD2/ANKK1 Taq Ia) had no effect on startle modulation. The findings support prior genetic and neuroimaging associations of the COMT 158Met allele to affective psychopathology and alterations in neural systems for emotional arousal and regulation.

The impact of chronic stress during adolescence on the development of aggressive behavior: A systematic review on the role of the dopaminergic system in rodents.

Pathological aggression, frequently observed in psychiatric patients and criminal subjects, poses a major burden on the health care and criminal justice system, necessitating better aetiological models to inform targets for prevention and intervention. Emerging evidence suggests that adverse experiences during development can cause long-lasting brain alterations associated with maladaptive behaviors, such as aggression. The present review discusses, mainly based on studies in rodents, whether disruption of the mesocorticolimbic dopamine system through chronic stress-exposure during adolescence predisposes to adult aggression. Our findings suggest that chronic stress in adolescence induces prefrontal cortex (PFC) hyperdopaminergia and ultimately leads to blunted prefrontal dopamine transmission in adulthood. This, in turn, disrupts the ability of the PFC to guide adaptive, long-term focused action selection by regulating mesolimbic dopamine signaling. We propose that, especially during the dynamic and transitional period of adolescence, exposure to chronic stress could lead to excessive adaptive change, which may result in an increased vulnerability to maladaptive aggression in adulthood. We discuss how these findings in rodents may translate to humans.

Predicting Violent Behavior: What Can Neuroscience Add?

The ability to accurately predict violence and other forms of serious antisocial behavior would provide important societal benefits, and there is substantial enthusiasm for the potential predictive accuracy of neuroimaging techniques. Here, we review the current status of violence prediction using actuarial and clinical methods, and assess the current state of neuroprediction. We then outline several questions that need to be addressed by future studies of neuroprediction if neuroimaging and other neuroscientific markers are to be successfully translated into public policy.

Blunted Ambiguity Aversion During Cost-Benefit Decisions in Antisocial Individuals.

Antisocial behavior is often assumed to reflect aberrant risk processing. However, many of the most significant forms of antisocial behavior, including crime, reflect the outcomes of decisions made under conditions of ambiguity rather than risk. While risk and ambiguity are formally distinct and experimentally dissociable, little is known about ambiguity sensitivity in individuals who engage in chronic antisocial behavior. We used a financial decision-making task in a high-risk community-based sample to test for associations between sensitivity to ambiguity, antisocial behavior, and arrest history. Sensitivity to ambiguity was lower in individuals who met diagnostic criteria for Antisocial Personality Disorder. Lower ambiguity sensitivity was also associated with higher externalizing (but not psychopathy) scores, and with higher levels of aggression (but not rule-breaking). Finally, blunted sensitivity to ambiguity also predicted a greater frequency of arrests. Together, these data suggest that alterations in cost-benefit decision-making under conditions of ambiguity may promote antisocial behavior.

Disrupted Prefrontal Regulation of Striatal Subjective Value Signals in Psychopathy.

Psychopathy is a personality disorder with strong links to criminal behavior. While research on psychopathy has focused largely on socio-affective dysfunction, recent data suggest that aberrant decision making may also play an important role. Yet, the circuit-level mechanisms underlying maladaptive decision making in psychopathy remain unclear. Here, we used a multi-modality functional imaging approach to identify these mechanisms in a population of adult male incarcerated offenders. Psychopathy was associated with stronger subjective value-related activity within the nucleus accumbens (NAcc) during inter-temporal choice and with weaker intrinsic functional connectivity between NAcc and ventromedial prefrontal cortex (vmPFC). NAcc-vmPFC connectivity strength was negatively correlated with NAcc subjective value-related activity; however, this putative regulatory pattern was abolished as psychopathy severity increased. Finally, weaker cortico-striatal regulation predicted more frequent criminal convictions. These data suggest that cortico-striatal circuit dysregulation drives maladaptive decision making in psychopathy, supporting the notion that reward system dysfunction comprises an important neurobiological risk factor.

Dysfunctional prefrontal regional specialization and compensation in schizophrenia.

OBJECTIVE: It has been suggested that in healthy persons higher-order cognitive processing engaged by incremental working memory load hierarchically employs more dorsal than ventral prefrontal resources in healthy individuals. Given that working memory performance is impaired in schizophrenia, especially at higher executive loads, the authors investigated how this prefrontal functional organization might be altered in disease, independent of performance deficits. METHOD: Using N-back working memory functional magnetic resonance imaging (fMRI) data, the authors studied 15 patients with schizophrenia and 26 healthy comparison subjects. Subgroups based on median performance accuracy at 2-back were analyzed; high performers included eight schizophrenia patients and 14 comparison subjects, and low performers included seven patients and 12 comparison subjects. RESULTS: High-performing but not low-performing comparison subjects responded to incremental working memory executive load with disproportionately greater dorsal but not ventral prefrontal cortex activation, which also predicted performance accuracy. In the high- and low-performing patient groups, incremental working memory load caused a disproportionate increase in ventral but not dorsal prefrontal cortex activation relative to the respective comparison group, which also correlated with accuracy. Functional connectivity between the ventral prefrontal cortex and posterior parietal cortex was relatively greater in patients, whereas comparison subjects had greater functional connectivity between the dorsal prefrontal cortex and posterior parietal cortex. CONCLUSIONS: The hierarchical organization of the prefrontal cortex may be compromised in schizophrenia, resulting in loss of functional specialization and integration at the dorsal prefrontal cortex and in compensatory activation from the ventral prefrontal cortex, which may ultimately affect working memory and executive cognition.

Selective Mapping of Psychopathy and Externalizing to Dissociable Circuits for Inhibitory Self-Control.

Antisociality is commonly conceptualized as a unitary construct, but there is considerable evidence for multidimensionality. In particular, two partially dissociable symptom clusters - psychopathy and externalizing - have divergent associations to clinical and forensic outcomes and are linked to unique patterns executive dysfunction. Here, we used fMRI in a sample of incarcerated offenders to map these dimensions of antisocial behavior to brain circuits underlying two aspects of inhibitory self-control: interference suppression and response inhibition. We found that psychopathy and externalizing are characterized by unique and task-selective patterns of dysfunction. While higher levels of psychopathy predicted increased activity within a distributed fronto-parietal network for interference suppression, externalizing did not predict brain activity during attentional control. By contrast, each dimension had opposite associations to fronto-parietal activity during response inhibition. These findings provide neurobiological evidence supporting the fractionation of antisocial behavior, and identify dissociable mechanisms through which different facets predispose dysfunction and impairment.