Parallel cognitive maps for multiple knowledge structures in the hippocampal formation.

The hippocampal-entorhinal system uses cognitive maps to represent spatial knowledge and other types of relational information. However, objects can often be characterized by different types of relations simultaneously. How does the hippocampal formation handle the embedding of stimuli in multiple relational structures that differ vastly in their mode and timescale of acquisition? Does the hippocampal formation integrate different stimulus dimensions into one conjunctive map or is each dimension represented in a parallel map? Here, we reanalyzed human functional magnetic resonance imaging data from Garvert et al. (2017) that had previously revealed a map in the hippocampal formation coding for a newly learnt transition structure. Using functional magnetic resonance imaging adaptation analysis, we found that the degree of representational similarity in the bilateral hippocampus also decreased as a function of the semantic distance between presented objects. Importantly, while both map-like structures localized to the hippocampal formation, the semantic map was located in more posterior regions of the hippocampal formation than the transition structure and thus anatomically distinct. This finding supports the idea that the hippocampal-entorhinal system forms parallel cognitive maps that reflect the embedding of objects in diverse relational structures.

Impulse control disorder in Parkinson's disease is associated with abnormal frontal value signalling.

Dopaminergic medication is well established to boost reward- versus punishment-based learning in Parkinson's disease. However, there is tremendous variability in dopaminergic medication effects across different individuals, with some patients exhibiting much greater cognitive sensitivity to medication than others. We aimed to unravel the mechanisms underlying this individual variability in a large heterogeneous sample of early-stage patients with Parkinson's disease as a function of comorbid neuropsychiatric symptomatology, in particular impulse control disorders and depression. One hundred and ninety-nine patients with Parkinson's disease (138 ON medication and 61 OFF medication) and 59 healthy controls were scanned with functional MRI while they performed an established probabilistic instrumental learning task. Reinforcement learning model-based analyses revealed medication group differences in learning from gains versus losses, but only in patients with impulse control disorders. Furthermore, expected-value related brain signalling in the ventromedial prefrontal cortex was increased in patients with impulse control disorders ON medication compared with those OFF medication, while striatal reward prediction error signalling remained unaltered. These data substantiate the hypothesis that dopamine's effects on reinforcement learning in Parkinson's disease vary with individual differences in comorbid impulse control disorder and suggest they reflect deficient computation of value in medial frontal cortex, rather than deficient reward prediction error signalling in striatum. See Michael Browning (https://doi.org/10.1093/brain/awad248) for a scientific commentary on this article.

Choice Boosts Curiosity.

In our connected era, we spend significant time and effort satisfying our curiosity. Often, we choose which information we seek, but sometimes the selection is made for us. We hypothesized that humans exhibit enhanced curiosity in the context of choice. We designed a task in which healthy participants saw two lotteries on each trial. On some trials, participants chose which lottery to play. On other trials, the lottery was selected for them. Participants then indicated their curiosity about the outcome of the to-be-played lottery via self-report ratings (Experiment 1, N = 34) or willingness-to-wait decisions (Experiment 2, N = 34). We found that participants exhibited higher curiosity ratings and greater willingness to wait for the outcome of lotteries they had chosen than for lotteries that had been selected for them (controlling for initial preference). This demonstrates that choice boosts curiosity, which may have implications for boosting learning, memory, and motivation.

Striatal BOLD and Midfrontal Theta Power Express Motivation for Action.

Action selection is biased by the valence of anticipated outcomes. To assess mechanisms by which these motivational biases are expressed and controlled, we measured simultaneous EEG-fMRI during a motivational Go/NoGo learning task (N = 36), leveraging the temporal resolution of EEG and subcortical access of fMRI. VmPFC BOLD encoded cue valence, importantly predicting trial-by-trial valence-driven response speed differences and EEG theta power around cue onset. In contrast, striatal BOLD encoded selection of active Go responses and correlated with theta power around response time. Within trials, theta power ramped in the fashion of an evidence accumulation signal for the value of making a "Go" response, capturing the faster responding to reward cues. Our findings reveal a dual nature of midfrontal theta power, with early components reflecting the vmPFC contribution to motivational biases, and late components reflecting their striatal translation into behavior, in line with influential recent "value of work" theories of striatal processing.

Challenging the negative learning bias hypothesis of depression: reversal learning in a naturalistic psychiatric sample.

BACKGROUND: Classic theories posit that depression is driven by a negative learning bias. Most studies supporting this proposition used small and selected samples, excluding patients with comorbidities. However, comorbidity between psychiatric disorders occurs in up to 70% of the population. Therefore, the generalizability of the negative bias hypothesis to a naturalistic psychiatric sample as well as the specificity of the bias to depression, remain unclear. In the present study, we tested the negative learning bias hypothesis in a large naturalistic sample of psychiatric patients, including depression, anxiety, addiction, attention-deficit/hyperactivity disorder, and/or autism. First, we assessed whether the negative bias hypothesis of depression generalized to a heterogeneous (and hence more naturalistic) depression sample compared with controls. Second, we assessed whether negative bias extends to other psychiatric disorders. Third, we adopted a dimensional approach, by using symptom severity as a way to assess associations across the sample. METHODS: We administered a probabilistic reversal learning task to 217 patients and 81 healthy controls. According to the negative bias hypothesis, participants with depression should exhibit enhanced learning and flexibility based on punishment v. reward. We combined analyses of traditional measures with more sensitive computational modeling. RESULTS: In contrast to previous findings, this sample of depressed patients with psychiatric comorbidities did not show a negative learning bias. CONCLUSIONS: These results speak against the generalizability of the negative learning bias hypothesis to depressed patients with comorbidities. This study highlights the importance of investigating unselected samples of psychiatric patients, which represent the vast majority of the psychiatric population.

Frontal network dynamics reflect neurocomputational mechanisms for reducing maladaptive biases in motivated action.

Motivation exerts control over behavior by eliciting Pavlovian responses, which can either match or conflict with instrumental action. We can overcome maladaptive motivational influences putatively through frontal cognitive control. However, the neurocomputational mechanisms subserving this control are unclear; does control entail up-regulating instrumental systems, down-regulating Pavlovian systems, or both? We combined electroencephalography (EEG) recordings with a motivational Go/NoGo learning task (N = 34), in which multiple Go options enabled us to disentangle selective action learning from nonselective Pavlovian responses. Midfrontal theta-band (4 Hz-8 Hz) activity covaried with the level of Pavlovian conflict and was associated with reduced Pavlovian biases rather than reduced instrumental learning biases. Motor and lateral prefrontal regions synchronized to the midfrontal cortex, and these network dynamics predicted the reduction of Pavlovian biases over and above local, midfrontal theta activity. This work links midfrontal processing to detecting Pavlovian conflict and highlights the importance of network processing in reducing the impact of maladaptive, Pavlovian biases.

Effects of dopamine on reinforcement learning in Parkinson's disease depend on motor phenotype.

Parkinson's disease is clinically defined by bradykinesia, along with rigidity and tremor. However, the severity of these motor signs is greatly variable between individuals, particularly the presence or absence of tremor. This variability in tremor relates to variation in cognitive/motivational impairment, as well as the spatial distribution of neurodegeneration in the midbrain and dopamine depletion in the striatum. Here we ask whether interindividual heterogeneity in tremor symptoms could account for the puzzlingly large variability in the effects of dopaminergic medication on reinforcement learning, a fundamental cognitive function known to rely on dopamine. Given that tremor-dominant and non-tremor Parkinson's disease patients have different dopaminergic phenotypes, we hypothesized that effects of dopaminergic medication on reinforcement learning differ between tremor-dominant and non-tremor patients. Forty-three tremor-dominant and 20 non-tremor patients with Parkinson's disease were recruited to be tested both OFF and ON dopaminergic medication (200/50 mg levodopa-benserazide), while 22 age-matched control subjects were recruited to be tested twice OFF medication. Participants performed a reinforcement learning task designed to dissociate effects on learning rate from effects on motivational choice (i.e. the tendency to 'Go/NoGo' in the face of reward/threat of punishment). In non-tremor patients, dopaminergic medication improved reward-based choice, replicating previous studies. In contrast, in tremor-dominant patients, dopaminergic medication improved learning from punishment. Formal modelling showed divergent computational effects of dopaminergic medication as a function of Parkinson's disease motor phenotype, with a modulation of motivational choice bias and learning rate in non-tremor and tremor patients, respectively. This finding establishes a novel cognitive/motivational difference between tremor and non-tremor Parkinson's disease patients, and highlights the importance of considering motor phenotype in future work.

Emotionally Aversive Cues Suppress Neural Systems Underlying Optimal Learning in Socially Anxious Individuals.

Learning and decision-making are modulated by socio-emotional processing and such modulation is implicated in clinically relevant personality traits of social anxiety. The present study elucidates the computational and neural mechanisms by which emotionally aversive cues disrupt learning in socially anxious human individuals. Healthy volunteers with low or high trait social anxiety performed a reversal learning task requiring learning actions in response to angry or happy face cues. Choice data were best captured by a computational model in which learning rate was adjusted according to the history of surprises. High trait socially anxious individuals used a less-dynamic strategy for adjusting their learning rate in trials started with angry face cues and unlike the low social anxiety group, their dorsal anterior cingulate cortex (dACC) activity did not covary with the learning rate. Our results demonstrate that trait social anxiety is accompanied by disruption of optimal learning and dACC activity in threatening situations.SIGNIFICANCE STATEMENT Social anxiety is known to influence a broad range of cognitive functions. This study tests whether and how social anxiety affects human value-based learning as a function of uncertainty in the learning environment. The findings indicate that, in a threatening context evoked by an angry face, socially anxious individuals fail to benefit from a stable learning environment with highly predictable stimulus-response-outcome associations. Under those circumstances, socially anxious individuals failed to use their dorsal anterior cingulate cortex, a region known to adjust learning rate to environmental uncertainty. These findings open the way to modify neurobiological mechanisms of maladaptive learning in anxiety and depressive disorders.

Methylphenidate does not affect convergent and divergent creative processes in healthy adults.

An increasing number of healthy people use methylphenidate, a psychostimulant that increases dopamine and noradrenaline transmission in the brain, to help them focus over extended periods of time. While methylphenidate has been shown to facilitate some cognitive functions, like focus and distractor-resistance, the same drug might also contribute to cognitive impairment, for example, in creativity. In this study, we investigated whether acute administration of a low oral dose (20 mg) of methylphenidate affected convergent and divergent creative processes in a sample of young healthy participants. Also, we explored whether such effects depended on individual differences in ADHD symptoms and working memory capacity. Contrary to our expectations, methylphenidate did not affect participants' creative performance on any of the tasks. Also, methylphenidate effects did not depend on individual differences in trait hyperactivity-impulsivity or baseline working memory capacity. Thus, although the effects of methylphenidate on creativity might be underestimated in our study due to several methodological factors, our findings do not suggest that methylphenidate impairs people's ability to be creative.

GABAergic changes in the thalamocortical circuit in Parkinson's disease.

Parkinson's disease is characterized by bradykinesia, rigidity, and tremor. These symptoms have been related to an increased gamma-aminobutyric acid (GABA)ergic inhibitory drive from globus pallidus onto the thalamus. However, in vivo empirical evidence for the role of GABA in Parkinson's disease is limited. Some discrepancies in the literature may be explained by the presence or absence of tremor. Specifically, recent functional magnetic resonance imaging (fMRI) findings suggest that Parkinson's tremor is associated with reduced, dopamine-dependent thalamic inhibition. Here, we tested the hypothesis that GABA in the thalamocortical motor circuit is increased in Parkinson's disease, and we explored differences between clinical phenotypes. We included 60 Parkinson patients with dopamine-resistant tremor (n = 17), dopamine-responsive tremor (n = 23), or no tremor (n = 20), and healthy controls (n = 22). Using magnetic resonance spectroscopy, we measured GABA-to-total-creatine ratio in motor cortex, thalamus, and a control region (visual cortex) on two separate days (ON and OFF dopaminergic medication). GABA levels were unaltered by Parkinson's disease, clinical phenotype, or medication. However, motor cortex GABA levels were inversely correlated with disease severity, particularly rigidity and tremor, both ON and OFF medication. We conclude that cortical GABA plays a beneficial rather than a detrimental role in Parkinson's disease, and that GABA depletion may contribute to increased motor symptom expression.

Induction and Relief of Curiosity Elicit Parietal and Frontal Activity.

Curiosity is a basic biological drive, but little is known about its behavioral and neural mechanisms. We can be curious about several types of information. On the one hand, curiosity is a function of the expected value of information, serving primarily to help us maximize reward. On the other hand, curiosity can be a function of the uncertainty of information, helping us to update what we know. In the current studies, we aimed to disentangle the contribution of information uncertainty and expected value of rewards to curiosity in humans. To this end, we designed a lottery task in which uncertainty and expected value of trial outcomes were manipulated independently and examined how neural activity and behavioral measures of curiosity were modulated by these factors. Curiosity increased linearly with increased outcome uncertainty, both when curiosity was explicitly probed as well as when it was implicitly tested by people's willingness to wait. Increased expected value, however, did not strongly relate to these curiosity measures. Neuroimaging results showed greater BOLD response with increasing outcome uncertainty in parietal cortex at the time of curiosity induction. Outcome updating when curiosity was relieved resulted in an increased signal in the insula, orbitofrontal cortex, and parietal cortex. Furthermore, the insula showed a linear increase corresponding to the size of the information update. These results suggest that curiosity is monotonically related to the uncertainty about one's current world model, the induction and relief of which are associated with activity in parietal and insular cortices, respectively.SIGNIFICANCE STATEMENT Humans are curious by nature. When you hear your phone beep, you probably feel the urge to check the message right away, even though the message itself likely does not give you a direct reward. In this study, we demonstrated that curiosity can be driven by outcome uncertainty, over and above of reward. The induction of curiosity was accompanied by increased activity in the parietal cortex, whereas the information update at the time of curiosity relief was associated with activity in insular cortex. These findings advance our understanding of the behavioral and neural constituents of curiosity, which lies at the core of human information seeking and serves to optimize the individual's current world model.

The contribution of striatal pseudo-reward prediction errors to value-based decision-making.

Most studies that have investigated the brain mechanisms underlying learning have focused on the ability to learn simple stimulus-response associations. However, in everyday life, outcomes are often obtained through complex behavioral patterns involving a series of actions. Parallel learning systems might be important to reduce the complexity of the learning problem in such scenarios, as proposed in the framework of hierarchical reinforcement learning (HRL). The key feature of HRL is the decomposition of complex sets of action into subgoals. These subgoals are associated with the computation of pseudo-reward prediction errors (PRPEs), which allow the reinforcement of actions that led to a subgoal before the final goal itself is achieved. Here we wanted to test the hypothesis that, despite not carrying any rewarding value per se, pseudo-rewards might generate a bias in choice behavior in the absence of any advantage. Second, we also hypothesized that this bias might be related to the strength of PRPE striatal representations. In order to test these ideas, we developed a novel decision-making paradigm to assess reward prediction errors (RPEs) and PRPEs in two studies (fMRI study: n = 20; behavioral study: n = 19). Our results show that the participants developed a preference for the most pseudo-rewarding option throughout the task, even though it did not lead to more monetary rewards. fMRI analyses revealed that this preference was predicted by individual differences in the relative striatal sensitivity to PRPEs vs RPEs. Together, our results indicate that pseudo-rewards generate learning signals in the striatum and subsequently bias choice behavior despite their lack of association with actual reward.

Occipital Alpha and Gamma Oscillations Support Complementary Mechanisms for Processing Stimulus Value Associations.

Selective attention is reflected neurally in changes in the power of posterior neural oscillations in the alpha (8-12 Hz) and gamma (40-100 Hz) bands. Although a neural mechanism that allows relevant information to be selectively processed has its advantages, it may lead to lucrative or dangerous information going unnoticed. Neural systems are also in place for processing rewarding and punishing information. Here, we examine the interaction between selective attention (left vs. right) and stimulus's learned value associations (neutral, punished, or rewarded) and how they compete for control of posterior neural oscillations. We found that both attention and stimulus-value associations influenced neural oscillations. Whereas selective attention had comparable effects on alpha and gamma oscillations, value associations had dissociable effects on these neural markers of attention. Salient targets (associated with positive and negative outcomes) hijacked changes in alpha power-increasing hemispheric alpha lateralization when salient targets were attended, decreasing it when they were being ignored. In contrast, hemispheric gamma-band lateralization was specifically abolished by negative distractors. Source analysis indicated occipital generators of both attentional and value effects. Thus, posterior cortical oscillations support both the ability to selectively attend while at the same time retaining the ability to remain sensitive to valuable features in the environment. Moreover, the versatility of our attentional system to respond separately to salient from merely positively valued stimuli appears to be carried out by separate neural processes reflected in different frequency bands.

Top-down expectation effects of food labels on motivation.

Labels on food packages inform our beliefs, shaping our expectations of food properties, such as its expected taste and healthiness. These beliefs can influence the processing of caloric rewards beyond objective sensory properties and have the potential to impact decision making. However, no studies, within or beyond the food domain, have assessed how written information, such as food labels, affect implicit motivation to obtain rewards, even though choices in daily life might be strongly driven by implicit motivational biases. We investigated how written information affects implicit motivation to obtain caloric rewards in healthy young adults. We used food labels (high- and low-calorie), associated with an identical fruit-flavored sugar-sweetened beverage, to study motivation for caloric rewards during fMRI. In a joystick task, hungry participants (N = 31) were instructed to make fast approach or avoid movements to earn the cued beverages. Behaviorally, we found a general approach bias, which was stronger for the beverage that was most preferred during a subsequent choice test, i.e., the one labeled as low-calorie. This behavioral effect was accompanied by increased BOLD signal in the sensorimotor cortex during the response phase of the task for the preferred, low-calorie beverage compared with the non-preferred, high-calorie beverage. During the anticipation phase, the non-preferred, high-calorie beverage label elicited stronger fMRI signal in the right ventral anterior insula, a region associated with aversion and taste intensity, than the preferred, low-calorie label. Together, these data suggest that high-calorie labeling can increase avoidance of beverages and reduce neural activity in brain regions associated with motor control. In conclusion, we show effects of food labeling on fMRI responses during anticipation and subsequent motivated action and on behavior, in the absence of objective taste differences, demonstrating the influence of written information on implicit biases. These findings contribute to our understanding of implicit biases in real-life eating behavior.

Enhanced motivation of cognitive control in Parkinson's disease.

Motor and cognitive deficits in Parkinson's disease (PD) have been argued to reflect motivational deficits. In prior work, however, we have shown that motivation of cognitive control is paradoxically potentiated rather than impaired in Parkinson's disease. This is particularly surprising given the fact that Parkinson's disease is often accompanied by depression, a prototypical disorder of motivation. To replicate our previous finding and assess the effects of depression, we investigated performance of PD patients with (n = 22) and without depression (history) (n = 23) and age-matched healthy controls (n = 23) on a task specifically designed to measure the effect of reward motivation on task-switching. We replicated previous findings by showing contrasting effects of reward motivation on task-switching in PD patients and age-matched healthy controls. While the promise of high versus low reward improved task-switching in PD, it tended to impair task-switching in age-matched healthy controls. There were no effects of a depression (history) diagnosis in PD patients. These findings reinforce prior observations that Parkinson's disease is accompanied by enhanced incentive motivation of cognitive control and highlight the potential of incentive motivational strategies for overcoming cognitive deficits in Parkinson's disease.

Spontaneous eye blink rate and dopamine synthesis capacity: preliminary evidence for an absence of positive correlation.

Dopamine is central to a number of cognitive functions and brain disorders. Given the cost of neurochemical imaging in humans, behavioural proxy measures of dopamine have gained in popularity in the past decade, such as spontaneous eye blink rate (sEBR). Increased sEBR is commonly associated with increased dopamine function based on pharmacological evidence and patient studies. Yet, this hypothesis has not been validated using in vivo measures of dopamine function in humans. To fill this gap, we measured sEBR and striatal dopamine synthesis capacity using [18 F]DOPA PET in 20 participants (nine healthy individuals and 11 pathological gamblers). Our results, based on frequentist and Bayesian statistics, as well as region-of-interest and voxel-wise analyses, argue against a positive relationship between sEBR and striatal dopamine synthesis capacity. They show that, if anything, the evidence is in favour of a negative relationship. These results, which complement findings from a recent study that failed to observe a relationship between sEBR and dopamine D2 receptor availability, suggest that caution and nuance are warranted when interpreting sEBR in terms of a proxy measure of striatal dopamine.

Dopaminergic Modulation of the Functional Ventrodorsal Architecture of the Human Striatum.

Interactions between motivational, cognitive, and motor regions of the striatum are crucial for implementing behavioral control. Work with experimental animals indicates that such interactions are sensitive to modulation by dopamine. Using systematic pharmacological manipulation of dopamine D2-receptors and resting-state functional imaging, we defined the functional architecture of the human striatum and quantified the effects of dopaminergic drugs on intrinsic effective connectivity between striatal subregions. We found that dopamine modulates interactions between motivational and cognitive regions, as well cognitive and motor regions of the striatum. Stimulation and blockade of the dopamine D2-receptor had opposite (increasing and decreasing) effects on the efficacy of those interactions. Furthermore, trait impulsivity was specifically associated with dopaminergic modulation of ventral-to-dorsal striatal connectivity. Individuals with high trait impulsivity exhibited greater drug-induced increases (after stimulation) and decreases (after blockade) of ventral-to-dorsal striatal connectivity than those with low trait impulsivity. These observations establish a key link between dopamine, intrinsic effective connectivity between striatal subregions, and trait impulsivity.

Human Choice Strategy Varies with Anatomical Projections from Ventromedial Prefrontal Cortex to Medial Striatum.

Two distinct systems, goal-directed and habitual, support decision making. It has recently been hypothesized that this distinction may arise from two computational mechanisms, model-based and model-free reinforcement learning, neuronally implemented in frontostriatal circuits involved in learning and behavioral control. Here, we test whether the relative strength of anatomical connectivity within frontostriatal circuits accounts for variation in human individuals' reliance on model-based and model-free control. This hypothesis was tested by combining diffusion tensor imaging with a multistep decision task known to distinguish model-based and model-free control in humans. We found large interindividual differences in the degree of model-based control, and those differences are predicted by the structural integrity of white-matter tracts from the ventromedial prefrontal cortex to the medial striatum. Furthermore, an analysis based on masking out of bottom-up tracts suggests that this effect is driven by top-down influences from ventromedial prefrontal cortex to medial striatum. Our findings indicate that individuals with stronger afferences from the ventromedial prefrontal cortex to the medial striatum are more likely to rely on a model-based strategy to control their instrumental actions. These findings suggest a mechanism for instrumental action control through which medial striatum determines, at least partly, the relative contribution of model-based and model-free systems during decision-making according to top-down model-based information from the ventromedial prefrontal cortex. These findings have important implications for understanding the neural circuitry that might be susceptible to pathological computational processes in impulsive/compulsive psychiatric disorders.

Stress and Cognitive Flexibility: Cortisol Increases Are Associated with Enhanced Updating but Impaired Switching.

Acute stress has frequently been shown to impair cognitive flexibility. Most studies have examined the effect of stress on cognitive flexibility by measuring how stress changes performance in paradigms that require participants to switch between different task demands. These processes typically implicate pFC function, a region known to be impaired by stress. However, cognitive flexibility is a multifaceted construct. Another dimension of flexibility, updating to incorporate relevant information, involves the dorsal striatum. Function in this region has been shown to be enhanced by stress. Using a within-subject design, we tested whether updating flexibility in a DMS task would be enhanced by an acute stress manipulation (cold pressor task). Participants' cortisol response to stress positively correlated with a relative increase in accuracy on updating flexibility (compared with trials with no working memory interference). In contrast, in line with earlier studies, cortisol responses correlated with worse performance when switching between trials with different task demands. These results demonstrate that stress-related increases in cortisol are associated with both increases and decreases in cognitive flexibility, depending on task demands.

The Neurocognitive Cost of Enhancing Cognition with Methylphenidate: Improved Distractor Resistance but Impaired Updating.

A balance has to be struck between supporting distractor-resistant representations in working memory and allowing those representations to be updated. Catecholamine, particularly dopamine, transmission has been proposed to modulate the balance between the stability and flexibility of working memory representations. However, it is unclear whether drugs that increase catecholamine transmission, such as methylphenidate, optimize this balance in a task-dependent manner or bias the system toward stability at the expense of flexibility (or vice versa). Here we demonstrate, using pharmacological fMRI, that methylphenidate improves the ability to resist distraction (cognitive stability) but impairs the ability to flexibly update items currently held in working memory (cognitive flexibility). These behavioral effects were accompanied by task-general effects in the striatum and opposite and task-specific effects on neural signal in the pFC. This suggests that methylphenidate exerts its cognitive enhancing and impairing effects through acting on the pFC, an effect likely associated with methylphenidate's action on the striatum. These findings highlight that methylphenidate acts as a double-edged sword, improving one cognitive function at the expense of another, while also elucidating the neurocognitive mechanisms underlying these paradoxical effects.