Reward Processing Networks Research Articles

Paediatric obesity and metabolic syndrome associations with cognition and the brain in youth: Current evidence and future directions.

Obesity and components of the metabolic syndrome (MetS) are associated with differences in brain structure and function and in general and food-related cognition in adults. Here, we review evidence for similar phenomena in children and adolescents, with a focus on the implications of extant research for possible underlying mechanisms and potential interventions for obesity and MetS in youth. Current evidence is limited by a relative reliance on small cross-sectional studies. However, we find that youth with obesity and MetS or MetS components show differences in brain structure, including alterations in grey matter volume and cortical thickness across brain regions subserving reward, cognitive control and other functions, as well as in white matter integrity and volume. Children with obesity and MetS components also show some evidence for hyperresponsivity of food reward regions and hyporesponsivity of cognitive control circuits during food-related tasks, altered brain responses to food tastes, and altered resting-state connectivity including between cognitive control and reward processing networks. Potential mechanisms for these findings include neuroinflammation, impaired vascular reactivity, and effects of diet and obesity on myelination and dopamine function. Future observational research using longitudinal measures, improved sampling strategies and study designs, and rigorous statistical methods, promises to further illuminate dynamic relationships and causal mechanisms. Intervention studies targeted at modifiable biological and behavioural factors associated with paediatric obesity and MetS can further inform mechanisms, as well as test whether brain and behaviour can be altered for beneficial outcomes.

Neuroimaging oxytocin modulation of social reward learning in schizophrenia.

Conventional pharmacological approaches have limited effectiveness for schizophrenia. There is interest in the application of oxytocin, which is involved in social cognition. Clinical trials have yielded mixed results, with a gap in understanding neural mechanisms. To evaluate the behavioural impact of oxytocin administration on a social learning task in individuals with schizophrenia, and elucidate any differential neural activity produced. We recruited 20 clinically stable right-handed men diagnosed with schizophrenia or schizoaffective disorder. In a double-blind cross-over randomised controlled study, 40 IU of oxytocin or placebo were administered before functional magnetic resonance imaging of participants playing a multi-round economic exchange game of trust. Participants had the role of investors (investment trials) receiving repayment on their investments (repayment trials), playing one session against a computer and a second against a player believed to be human. During investment trials, oxytocin increased neural signalling in the right lateral parietal cortex for both human and computer player trials, and attenuated signalling in the right insula for human player trials. For repayment trials, oxytocin elicited signal increases in left insula and left ventral caudate, and a signal decrease in right amygdala during the human player trials; conversely it resulted in right dorsal caudate activation during the computer player trials. We did not find a significant change in behavioural performance associated with oxytocin administration, or any associations with symptoms. During a social learning task oxytocin modulates cortical and limbic substrates of the reward-processing network. These perturbations can be putatively linked to the pathoaetiology of schizophrenia.

Intrinsic Connectivity and Family Dynamics: Striatolimbic Markers of Risk and Resilience in Youth at Familial Risk for Mood Disorders

BackgroundFew studies to date have characterized functional connectivity (FC) within emotion and reward networks in relation to family dynamics in youth at high familial risk for bipolar disorder (HR-BD) and major depressive disorder (HR-MDD) relative to low-risk youth (LR). Such characterization may advance our understanding of the neural underpinnings of mood disorders and lead to more effective interventions. MethodsA total of 139 youth (43 HR-BD, 46 HR-MDD, and 50 LR) aged 12.9 ± 2.7 years were longitudinally followed for 4.5 ± 2.4 years. We characterized differences in striatolimbic FC that distinguished between HR-BD, HR-MDD, and LR and between resilience and conversion to psychopathology. We then examined whether risk status moderated FC–family dynamic associations. Finally, we examined whether baseline between-group FC differences predicted resilence versus conversion to psychopathology. ResultsHR-BD had greater amygdala–middle frontal gyrus and dorsal striatum–middle frontal gyrus FC relative to HR-MDD and LR, and HR-MDD had lower amygdala–fusiform gyrus and dorsal striatum–precentral gyrus FC relative to HR-BD and LR (voxel-level p < .001, cluster-level false discovery rate–corrected p < .05). Resilient youth had greater amygdala–orbitofrontal cortex and ventral striatum–dorsal anterior cingulate cortex FC relative to youth with conversion to psychopathology (voxel-level p < .001, cluster-level false discovery rate–corrected p < .05). Greater family rigidity was inversely associated with amygdala–fusiform gyrus FC across all groups (false discovery rate–corrected p = .017), with a moderating effect of bipolar risk status (HR-BD vs. HR-MDD p < .001; HR-BD vs. LR p = .005). Baseline FC differences did not predict resilence versus conversion to psychopathology. ConclusionsFindings represent neural signatures of risk and resilience in emotion and reward processing networks in youth at familial risk for mood disorders that may be targets for novel interventions tailored to the family context.

Nucleus accumbens microstructure mediates the relationship between obesity and eating behavior in adults.

Basal ganglia regions are part of the brain's reward-processing networks and are implicated in the neurobiology of obesity and eating disorders. This study examines basal ganglia microstructural properties in adults with and without obesity. Diffusion basis spectrum imaging (DBSI) images were analyzed to obtain putative imaging markers of neuroinflammation. Relationships between basal ganglia DBSI metrics and reward sensitivity and eating behaviors were also explored. A total of 46 participants (25 people with obesity; aged 20-40 years; 37 women) were included. Relative to the people in the normal-weight group, people with obesity had smaller caudate and larger nucleus accumbens (NAcc) volumes (p < 0.05) and lower DBSI fiber fraction (reflecting apparent axonal/dendrite density) in NAcc and putamen, higher DBSI nonrestricted fraction (reflecting tissue edema) in NAcc and caudate, and higher DBSI restricted fraction (reflecting tissue cellularity) in putamen (p ≤ 0.01, all). Increased emotional and reward eating behaviors were related to lower NAcc axonal/dendrite density and greater tissue edema (p ≤ 0.002). The relationships between emotional eating and adiposity measures were mediated by NAcc microstructure. These findings provide evidence that microstructural alterations in basal ganglia relate to obesity and insights linking NAcc microstructure and eating behavior in adults.

Altered regional grey matter volume and appetite-related hormone levels in adolescent obesity with or without binge-eating disorder.

Binge eating disorder (BED) is characterized by frequent and persistent overeating episodes of binge eating without compensatory behaviors. The aim was to evaluate regional gray matter volume (GMV) abnormalities and appetite-regulating hormone levels (NPY and Leptin) in obese subjects either with or without BED compared to healthy controls (HC). Twenty-six obese patients with BED, 25 obese patients without BED and 27 healthy subjects as an age-matched control group with neuroimaging and appetite-regulating hormone levels were found eligible for regional GMV abnormalities. A structural magnetic resonance scan and timely blood samples were drawn to assess the appetite-regulating hormone levels. The BED obese patients had a greater GMVs of the right medial orbitofrontal cortex (OFC) and the left medial OFC compared to the non-BED obese patients. BED patients were characterized by greater GMV of the left medial OFC than HCs. Relative to the HCs, higher serum NPY levels were found in BED obese and non-BED obese groups. Serum leptin levels (pg/mL) had positively correlations with GMV in right medial OFC, left medial OFC, right lateral OFC, and left anterior cingulate cortex. Among the reward processing network, which is largely associated with feeding behaviours in individuals with obesity and binge eating disorder, the OFC volumes was correlated with serum leptin concentrations. The results of our study may provide a rationale for exploring the link between regional grey matter volumes and appetite-related hormone levels in people with BED. Level III, case-control analytic study.

Effects of Parenting Environment on Child and Adolescent Social-Emotional Brain Function.

The caregiving environment that children and adolescents experience is critically important for their social-emotional development. Parenting may affect child social-emotional outcomes through its effects in shaping the child's developing brain. Research has begun to investigate effects of parenting on child and adolescent brain function in humans using functional magnetic resonance imaging (fMRI). Here we review these initial studies. These studies find associations between parenting behavior and child and adolescent functional activation in neural networks involved in emotional arousal, emotion regulation (ER), reward processing, cognitive control, and social-emotional information processing. Findings from these studies suggest that higher negative parenting and lower positive parenting are generally associated with heightened activation in emotional arousal networks in response to negative emotional stimuli in youth. Further, findings indicate that lower positive parenting is associated with higher response in reward processing networks to monetary reward in youth. Finally, findings show that lower positive parenting predicts lower activation in cognitive control networks during cognitive control tasks and less adaptive neural responses to parent-specific stimuli. Several studies found these associations to be moderated by child sex or psychopathology risk status and we discuss these moderating factors and discuss implications of findings for children's social-emotional development.

The impact of familial risk and early life adversity on emotion and reward processing networks in youth at-risk for bipolar disorder.

A recently developed risk calculator for bipolar disorder (BD) accounts for clinical and parental psychopathology. Yet, it is understood that both familial predisposition and early life adversity contribute to the development of BD. How the interplay between these two factors influence emotion and reward processing networks in youth at risk for BD remains unclear. In this exploratory analysis, offspring of BD parents performed emotion and reward processing tasks while undergoing a fMRI scan. Risk calculator score was used to assess risk for developing BD in the next 5 years. Environmental risk was tabulated using the Stressful Life Events Schedule (SLES). Emotion and reward processing networks were investigated for genetic and/or environment interactions. Interaction effects were found between risk calculator scores, negative SLES score and activity in right amygdala and bilateral fusiform gyri during the emotion processing task, as well as activity in the fronto-, striatal, and parietal regions during the reward processing task. Our findings are preliminary; however, they support the unique and interactive contributions of both familial and environmental risk factors on emotion and reward processing within OBP. They also identify potential neural targets to guide development of interventions for youth at greatest risk for psychiatric disorders.

Dopamine and reward: a view from the prefrontal cortex.

The prefrontal cortex (PFC) is a heterogeneous area that is critical to reward-based decision-making. In particular, the dorsal anterior cingulate cortex, ventromedial PFC and orbitofrontal cortex are frequently implicated in different aspects of choice behaviour. These regions receive projections from midbrain dopamine (DA) neurons and, in turn, project to other key dopaminergic regions such as the striatum. However, our current understanding of the role of DA in reward-based processes is based mainly on studies of midbrain dopaminergic neurons and striatal DA release from nonhuman animal models. An important gap in the literature surrounds the precise functions of DA release in the PFC, particularly in humans. A priority for future research will be to integrate, both computationally and biologically, the seemingly disparate value representations across different nodes within the reward-processing network. Such models should aim to define the functional interactions between the PFC and basal ganglia, through which dopaminergic neurotransmission guides reward-based behaviour.

Brain intrinsic network connectivity in individuals with frequent tanning behavior

ABSTRACTBackground: Emergent studies suggest a bidirectional relationship between brain functioning and the skin. This neurocutaneous connection may be responsible for the reward response to tanning and, thus, may contribute to excessive tanning behavior. To date, however, this association has not yet been examined. Objectives: To explore whether intrinsic brain functional connectivity within the default mode network (DMN) is related to indoor tanning behavior. Methods: Resting state functional connectivity (rsFC) was obtained in twenty adults (16 females) with a history of indoor tanning. Using a seed-based [(posterior cingulate cortex (PCC)] approach, the relationship between tanning severity and FC strength was assessed. Tanning severity was measured with symptom count from the Structured Clinical Interview for Tanning Abuse and Dependence (SITAD) and tanning intensity (lifetime indoor tanning episodes/years tanning). Results: rsFC strength between the PCC and other DMN regions (left globus pallidus, left medial frontal gyrus, left superior frontal gyrus) is positively correlated with tanning symptom count. rsFC strength between the PCC and salience network regions (right anterior cingulate cortex, left inferior parietal lobe, left inferior temporal gyrus) is correlated with tanning intensity. Conclusion: Greater connectivity between tanning severity and DMN and salience network connectivity suggests that heightened self-awareness of salient stimuli may be a mechanism that underlies frequent tanning behavior. These findings add to the growing evidence of brain-skin connection and reflect dysregulation in the reward processing networks in those with frequent tanning.

Preliminary evidence for genetic overlap between body mass index and striatal reward response

The reward-processing network is implicated in the aetiology of obesity. Several lines of evidence suggest obesity-linked genetic risk loci (such as DRD2 and FTO) may influence individual variation in body mass index (BMI) through neuropsychological processes reflected in alterations in activation of the striatum during reward processing. However, no study has tested the broader hypotheses that (a) the relationship between BMI and reward-related brain activation (measured through the blood oxygenation-dependent (BOLD) signal) may be observed in a large population study and (b) the overall genetic architecture of these phenotypes overlap, an assumption critical for the progression of imaging genetic studies in obesity research. Using data from the Human Connectome Project (N = 1055 healthy, young individuals: average BMI = 26.4), we first establish a phenotypic relationship between BMI and ventral striatal (VS) BOLD during the processing of rewarding (monetary) stimuli (β = 0.44, P = 0.013), accounting for potential confounds. BMI and VS BOLD were both significantly influenced by additive genetic factors (H2r = 0.57; 0.12, respectively). Further decomposition of this variance suggested that the relationship was driven by shared genetic (ρg = 0.47, P = 0.011), but not environmental (ρE = −0.07, P = 0.29) factors. To validate the assumption of genetic pleiotropy between BMI and VS BOLD, we further show that polygenic risk for higher BMI is also associated with increased VS BOLD response to appetitive stimuli (calorically high food images), in an independent sample (N = 81; PFWE−ROI < 0.005). Together, these observations suggest that the genetic factors link risk to obesity to alterations within key nodes of the brain's reward circuity. These observations provide a basis for future work exploring the mechanistic role of genetic loci that confer risk for obesity using the imaging genetics approach.

Theta, Alpha and Beta Band Modulations During Auditory Condensation Task Performance

Outcome of a behavioral response can be detected either internally at the time of the response commission, or externally through a feedback signal. In both cases, a number of brain networks that subserve cognitive control are recruited, all networks having certain distinctive signatures in electroencephalographic oscillations. Yet most studies in the field have several limitations. First, typical behavioral tasks depend heavily upon inhibition of prepotent responses – thus they mostly exploit control of the motor threshold rather than the full range of processes related to cognitive control. Second, these studies were conducted in the visual modality, leaving it unclear whether the oscillatory phenomena found in these studies truly relate to cognitive control or they reflect effects specific to the tasks used. Here, we studied outcome-related adjustments by analyzing response-related and feedback-related modulations of theta, alpha, and beta band activity in the auditory version of the condensation task, which bears no inherent dependence upon inhibition of prepotent responses and which is administered in the auditory modality. Frontal midline theta (FMT) activity was enhanced after errors compared with correct trials, and after negative feedback compared with positive feedback. Alpha band suppression in the parieto-occipital region was enhanced in the late post-error interval. Frontal beta oscillatory activity was increased on correct trials during positive feedback onset. These findings indicate that several separate neuronal networks are involved in post-error and post-feedback adjustments: the midfrontal performance monitoring network, the parietal attentional network, and the frontal reward-processing network. Our findings extend the current knowledge concerning the functional role of theta, alpha, and beta band oscillations in cognitive control beyond a limited range of tasks and beyond the visual modality.

Neuroimaging the neural correlates of increased risk for substance use disorders in attention-deficit/hyperactivity disorder-A systematic review

Children with attention-deficit/hyperactivity disorder (ADHD) are nearly three times more likely to develop substance use disorders (SUD) than their typically developing peers. Our objective was to review the existing neuroimaging research on high-risk ADHD (ie, ADHD with disruptive behavior disorders, familial SUD and/or early substance use), focusing on impulsivity as one possible mechanism underlying SUD risk. A PubMed literature search was conducted using combinations of the keywords "ADHD," "substance use," "substance use disorder," "SUD," "addiction," "dependence," "abuse," "risk," "brain" "MRI," "imaging" and "neuroimaging." Studies had to include cohorts that met diagnostic criteria for ADHD; studies of individuals with ADHD who all met criteria for SUD were excluded. Eight studies met the search criteria. Individuals with high-risk ADHD have hyperactivation in the motivation-reward processing brain network during tasks of impulsive choice, emotion processing, and risky decision-making. During response inhibition tasks, they have hypoactivation in the inhibitory control brain network. However, studies focusing on this latter circuit found hypoactivation during inhibitory control tasks, decreased white matter microstructure coherence and reduced cortical thickness in ADHD independent of substance use history. An exaggerated imbalance between the inhibitory control network and the motivation-reward processing network is theorized to distinguish individuals with high-risk ADHD. Preliminary findings suggest that an exaggerated aberrant reward processing network may be the driving neural correlate of increased SUD risk in ADHD. Neural biomarkers of increased SUD risk in ADHD could help clinicians identify which patients may benefit most from SUD prevention. Thus, more neuroimaging research on this vulnerable population is needed. (Am J Addict 2017;26:99-111).

Neural alterations of fronto-striatal circuitry during reward anticipation in euthymic bipolar disorder.

Bipolar disorder (BD), with the hallmark symptoms of elevated and depressed mood, is thought to be characterized by underlying alterations in reward-processing networks. However, to date the neural circuitry underlying abnormal responses during reward processing in BD remains largely unexplored. The aim of this study was to investigate whether euthymic BD is characterized by aberrant ventral striatal (VS) activation patterns and altered connectivity with the prefrontal cortex in response to monetary gains and losses. During functional magnetic resonance imaging 20 euthymic BD patients and 20 age-, gender- and intelligence quotient-matched healthy controls completed a monetary incentive delay paradigm, to examine neural processing of reward and loss anticipation. A priori defined regions of interest (ROIs) included the VS and the anterior prefrontal cortex (aPFC). Psychophysiological interactions (PPIs) between these ROIs were estimated and tested for group differences for reward and loss anticipation separately. BD participants, relative to healthy controls, displayed decreased activation selectively in the left and right VS during anticipation of reward, but not during loss anticipation. PPI analyses showed decreased functional connectivity between the left VS and aPFC in BD patients compared with healthy controls during reward anticipation. This is the first study showing decreased VS activity and aberrant connectivity in the reward-processing circuitry in euthymic, medicated BD patients during reward anticipation. Our findings contrast with research supporting a reward hypersensitivity model of BD, and add to the body of literature suggesting that blunted activation of reward processing circuits may be a vulnerability factor for mood disorders.

Brain networks sub-serving self-referential processing in depression

IntroductionPersistent pondering over negative self-related thoughts is a central feature of depressive psychopathology.ObjectivesIn the present study, we sought to investigate the neural correlates of abnormal negative self-referential processing (SRP) in patients with major depressive disorder (MDD) and its impact on subsequent cognitive control-related neuronal activation.AimsWe hypothesized aberrant activation dynamics during the period of negative and neutral SRP in the rostral anterior cingulate cortex (rACC) and in the amygdala in patients with MDD. We assumed abnormal activation in the fronto-cingulate network during Stroop task execution.MethodsNineteen depressed patients and 20 healthy controls participated in the study. Using an event-related fMRI design, negative, positive and neutral self-referential statements were displayed for 6.5s and followed by incongruent or congruent Stroop conditions.ResultsIn contrast to controls, patients did not exhibit valence-dependent rACC activation differences during SRP. A novel finding was the significant activation of the amygdala and the reward-processing network during presentation of neutral self-referential stimuli relative to baseline and to affective stimuli in patients. The fMRI analysis of the Stroop task revealed a reduced BOLD activation in the right frontoparietal network of patients in the incongruent condition after negative SRP only.ConclusionsThus, the inflexible activation in the rACC may correspond to the inability of depressed patients to shift their attention away from negative self-related stimuli. The accompanying negative affect and task-irrelevant emotional processing may compete for neuronal resources with cognitive control processes and lead thereby to deficient cognitive performance associated with decreased frontoparietal activation.Disclosure of interestThe authors have not supplied their declaration of competing interest.

The neural basis of the abnormal self-referential processing and its impact on cognitive control in depressed patients.

Persistent pondering over negative self-related thoughts is a central feature of depressive psychopathology. In this study, we sought to investigate the neural correlates of abnormal negative self-referential processing (SRP) in patients with Major Depressive Disorder and its impact on subsequent cognitive control-related neuronal activation. We hypothesized aberrant activation dynamics during the period of negative and neutral SRP in the rostral anterior cingulate cortex (rACC) and in the amygdala in patients with major depressive disorder. Additionally, we assumed abnormal activation in the fronto-cingulate network during Stroop task execution. 19 depressed patients and 20 healthy controls participated in the study. Using an event-related functional magnetic resonance imaging (fMRI) design, negative, positive and neutral self-referential statements were displayed for 6.5 s and followed by incongruent or congruent Stroop conditions. The data were analyzed with SPM8. In contrast to controls, patients exhibited no significant valence-dependent rACC activation differences during SRP. A novel finding was the significant activation of the amygdala and the reward-processing network during presentation of neutral self-referential stimuli relative to baseline and to affective stimuli in patients. The fMRI analysis of the Stroop task revealed a reduced BOLD activation in the right fronto-parietal network of patients in the incongruent condition after negative SRP only. Thus, the inflexible activation in the rACC may correspond to the inability of depressed patients to shift their attention away from negative self-related stimuli. The accompanying negative affect and task-irrelevant emotional processing may compete for neuronal resources with cognitive control processes and lead thereby to deficient cognitive performance associated with decreased fronto-parietal activation.

Resting‐State Synchrony in Short‐Term Versus Long‐Term Abstinent Alcoholics

We previously reported that when compared with controls, long-term abstinent alcoholics (LTAA) have increased resting-state synchrony (RSS) of the inhibitory control network and reduced synchrony of the appetitive drive network, and hypothesized that these levels of synchrony are adaptive and support the behavioral changes required to maintain abstinence. In this study, we investigate whether these RSS patterns can be identified in short-term abstinent alcoholics (STAA). Resting-state functional magnetic resonance imaging data were collected from 27 STAA, 23 LTAA, and 23 nonsubstance abusing controls (NSAC). We examined baseline RSS using seed-based measures. We found ordered RSS effects from NSAC to STAA and then to LTAA within both the appetitive drive and executive control networks: increasing RSS of the executive control network and decreasing RSS of the reward processing network. Finally, we found significant correlations between strength of RSS in these networks and (i) cognitive flexibility, and (ii) current antisocial behavior. Findings are consistent with an adaptive progression of RSS from short- to long-term abstinence, so that, compared with normal controls, the synchrony (i) within the reward network progressively decreases, and (ii) within the executive control network progressively increases.

Developmental effects of reward on sustained attention networks

Adolescence is typified by significant maturation in higher-level attention functions coupled with less developed control over motivation, and enhanced sensitivity to novelty and reward.This study used event-related functional magnetic resonance imaging (fMRI) in seventy male and female participants aged between 10 and 43years to identify age-related linear changes in cognitive sustained attention systems and the impact of reward on these systems, using a sustained attention task with and without a rewarded condition.For the non-rewarded sustained attention contrast, increasing age was associated with activation increases in typical regions of sustained attention including right inferior frontal, superior temporo-parietal and cerebellar cortices. Age-related activation decreases were observed within more posterior regions including posterior cingulate, insula and posterior cerebellar cortices, presumably mediating visual–spatial saliency detection.The effect of reward on sustained attention networks was associated with increased activation with age in regions associated with both executive attention control and reward processing, including dorsolateral, inferior and ventromedial prefrontal cortices (PFC), striatum, and temporo-parietal regions, suggestive of greater integration and executive control of motivation and cognition with maturity. Activation in paralimbic posterior cingulate and inferior temporal brain regions of visual–spatial saliency processing was progressively reduced in activation with increasing development. Thus, with increasing development between adolescence and adulthood, reward appears to enhance maturing cognitive sustained attention and executive reward-processing networks, whilst reducing paralimbic regions of saliency detection. These findings may be the neural underpinnings for the progressive maturation of motivational control over risk taking behaviours between adolescence and adulthood.

Functional neuroimaging in anorexia nervosa: A clinical approach

Aims To provide a review of the available literature about the functional neuroimaging of anorexia nervosa, and to summarize the possible role of neurobiological factors in its pathogenesis. Methods A systematic review of the literature was performed using PubMed and Medline electronic database (1950–September 2009). Eligible studies were restricted to those involving the main parameters of cerebral activity and functional neuroimaging techniques. Findings of the reviewed studies have been grouped on a diagnostic subtype basis, and their comparison has been interpreted in terms of concordance. Results We found a high level of concordance among available studies with regard to the presence of frontal, parietal and cingulate functional disturbances in both anorexia nervosa restricting and binge/purging subtypes. Concordance among studies conducted regardless of the anorexia nervosa subtypes suggests an alteration in temporal and parietal functions and striatal metabolism. Conclusions The most consistent alterations in anorexia nervosa cerebral activity seem to involve the dorsolateral prefrontal cortex, the inferior parietal lobule, the anterior cingulate cortex and the caudate nucleus. They may affect different neural systems such as the frontal visual system, the attention network, the arousal and emotional processing systems, the reward processing network, and the network for the body schema.

Remedial effects of motivational incentive on declining cognitive control in healthy aging and Parkinson’s disease

The prospect of reward may provide a motivational incentive for optimizing goal-directed behavior. Animal work demonstrates that reward-processing networks and oculomotor-control networks in the brain are connected through the dorsal striatum, and that reward anticipation can improve oculomotor control via this nexus. Due perhaps to deterioration in dopaminergic striatal circuitry, goal-directed oculomotor control is subject to decline in healthy seniors, and even more in individuals with Parkinson's disease (PD). Here we examine whether healthy seniors and PD patients are able to utilize reward prospects to improve their impaired antisaccade performance. Results confirmed that oculomotor control declined in PD patients compared to healthy seniors, and in healthy seniors compared to young adults. However, the motivational incentive of reward expectation resulted in benefits in antisaccade performance in all groups alike. These findings speak against structural and non-modifiable decline in cognitive control functions, and emphasize the remedial potential of motivational incentive mechanisms in healthy as well as pathological aging.