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Growing evidence highlights the potential of innovative rehabilitative interventions such as cognitive remediation and neuromodulation, aimed at reducing relapses in Alcohol Use Disorder (AUD). Enhancing their effectiveness requires a thorough description of the neural correlates of cognitive alterations in AUD. Past related attempts, however, were limited by the focus on selected neuro-cognitive variables. We aimed to fill this gap by combining, in 22 AUD patients and 18 controls, an extensive neuro-cognitive evaluation and metrics of intrinsic connectivity as highlighted by resting-state brain activity. We addressed an inherent property of intrinsic activity such as intra-network coherence, the temporal correlation of the slow synchronous fluctuations within resting-state networks, representing an early biomarker of alterations in the functional brain architecture underlying cognitive functioning. AUD patients displayed executive impairments involving working-memory, attention and visuomotor speed, reflecting abnormal coherence of activity and grey matter atrophy within default mode, in addition to the attentional and the executive networks. The stronger relationship between fronto-lateral coherent activity and executive performance in patients than controls highlighted possible compensatory mechanisms counterbalancing the decreased functionality of networks driving the switch from automatic to controlled behavior. These results provide novel insights into AUD patients’ cognitive impairments, their neural bases, and possible targets of rehabilitative interventions.

Decreased punishment sensitivity in alcohol use disorder (AUD) might reflect a reduction in the typical human tendency to overweigh negative choice outcomes compared with equivalent positive ones, that is, ‘loss aversion.’ While this hypothesis is supported by previous reports of reduced loss aversion in AUD, it is still unknown whether such decreased sensitivity to prospective losses represents a specific facet of altered decision-making or a secondary effect of executive/working-memory impairments. We addressed this issue by assessing whether lower loss aversion in 22 AUD patients compared with 19 healthy controls is explained by their differential executive or working-memory performance and by investigating its neural basis in terms of grey matter density and cortical thickness via voxel- and surface-based morphometry, respectively. A significant decrease of loss aversion in patients, unrelated to their impaired executive/working-memory performance, reflected the reduction of posterior fronto-medial grey matter density and right frontopolar cortical thickness. Rather than their executive deficits, patients' reduced loss aversion reflects the structural damage of the posterior fronto-medial cortex previously associated with solving conflicts at the response level, where earlier functional magnetic resonance imaging (fMRI) studies have shown a ‘neural loss aversion’ pattern of steeper deactivation for losses than activation for gains, and of the frontopolar cortex in charge of managing competing goals. These findings highlight possible directions for addressing AUD patients' high relapse rate, for example, cognitive-behavioural rehabilitative interventions enhancing the awareness of the adverse outcomes of addiction or neurostimulation protocols targeting the regions processing their salience.

Despite the ubiquitous interdependence between one's own decisions and others' welfare, and the controversial evidence on the behavioral effect of choosing for others, the neural bases of making decisions for another versus oneself remain unexplored. We investigated whether loss aversion (LA; the tendency to avoid losses over approaching equivalent gains) is modulated by (i) choosing for oneself, other individuals, or both; (ii) knowing or not knowing the other recipients; or (iii) an interaction between these factors. We used fMRI to assess the brain activations associated with choosing whether to accept or reject mixed gambles, either for oneself, for another player, or both, in 2 groups of 28 participants who had or had not briefly interacted with the other players before scanning. Participants displayed higher LA for choices involving their payoff compared with those affecting only the payoff of other, known, players. This "social" modulation of decision-making was found to engage the dorsomedial prefrontal cortex and its inhibitory connectivity to the middle cingulate cortex. This pattern might underpin decision-making for known others via self-other distinction processes associated with dorsomedial prefrontal areas, with this in turn promoting the inhibition of socially oriented responses through the downregulation of the midcingulate node of the empathy network.

Mental flexibility (MF) has long been defined as cognitive flexibility. Specifically, it has been mainly studied within the executive functions domain. However, there has recently been increased attention towards its affective and physiological aspects. As a result, MF has been described as an ecological and cross-subject skill consisting of responding variably and flexibly to environmental cognitive-affective demands. Cross-sectional studies have mainly focused on samples composed of healthy individual and of patients with chronic conditions such as Mild Cognitive Impairment and Parkinson’s, emphasizing their behavioral rigidity. Our study is the first to consider a sample of healthy older subjects and to outline physiological and psychological markers typical of mental flexibility, to identify functional biomarkers associated with successful aging. Our results reveal that biomarkers (respiratory and heart rate variability assessments) distinguished between individuals high vs. low in mental flexibility more reliably than traditional neuropsychological tests. This unveiled the multifaceted nature of mental flexibility composed of both cognitive and affective aspects, which emerged only if non-linear multi-variate analytic approaches, such as Supervised Machine Learning, were used.

Older adults have been reported to have increased susceptibility to the adverse effects of SARS-CoV-2 infection, such as fatal outcomes, cognitive decline, and changes in physical and/or mental health. However, few studies have examined neuropsychological changes by comparing measurements before and during the pandemic in healthy older people. In addition, no longitudinal studies have examined whether older adults may have responded positively to the pandemic. We examined these issues through a 2-year neuropsychological study before and during the pandemic period. Results showed that scores before and during the pandemic were the same in memory and attention, whereas global cognitive, executive, and language functions improved. Participants also showed no longitudinal changes in depression, hypomania, and disinhibition, while apathy and, to a lesser extent, anxiety increased significantly. To examine possible signs of pandemic-related emotional (dys)regulation, subjects were shown images at follow-up that recalled the most dramatic lockdown phase while heart rate variability was recorded. Higher apathy was predicted by poorer global cognitive performance, increased anxiety, and emotional dysregulation as measured by a higher ratio of low-to-high frequency heart rate variability. Thus, preserved global cognition appears to play a protective role against the effects of pandemic-related anxiety and emotional dysregulation on apathy.

Increased decision latency in alcohol use disorder (AUD) has been generally explained in terms of psychomotor slowing. Recent results suggest that AUD patients’ slowed decision-making might rather reflect alterations in the neural circuitry underlying the engagement of controlled processing by salient stimuli. We addressed this hypothesis by testing a relationship between decision latency at the Cambridge Gambling Task (CGT) and intrinsic brain activity in 22 individuals with AUD and 19 matched controls. CGT deliberation time was related to two complementary facets of resting-state fMRI activity, i.e. coherence and intensity, representing early biomarkers of functional changes in the intrinsic brain architecture. For both metrics, we assessed a multiple regression (to test a relationship with deliberation time in the whole sample), and an interaction analysis (to test a significantly different relationship with decision latency across groups). AUD patients’ slowed deliberation time (p < 0.025) reflected distinct facets of altered intrinsic activity in the cingulate node of the anterior salience network previously associated with the “output” motor stage of response selection. Its heightened activity in AUD patients compared with controls, tracking choice latency (p < 0.025 corrected), might represent a compensation mechanism counterbalancing the concurrent decrease of its internal coherent activity (p < 0.025 corrected). These findings provide novel insights into the intrinsic neural mechanisms underlying increased decision latency in AUD, involving decreased temporal synchronicity in networks promoting executive control by behaviourally relevant stimuli. These results pave the way to further studies assessing more subtle facets of decision-making in AUD, and their possible changes with rehabilitative treatment.

Alcohol Use Disorder (AUD) is a chronic relapsing condition characterized by excessive alcohol consumption despite its multifaceted adverse consequences, associated with impaired performance in several cognitive domains including decision-making. While choice deficits represent a core component of addictive behavior, possibly consecutive to brain changes preceding the onset of the addiction cycle, the evidence on grey-matter and white-matter damage underlying abnormal choices in AUD is still limited. To fill this gap, we assessed the neurostructural bases of decision-making performance in 22 early-abstinent alcoholic patients and 18 controls, by coupling the Cambridge Gambling Task (CGT) with quantitative magnetic resonance imaging metrics of grey-matter density and white-matter integrity. Regardless of group, voxel based morphometry highlighted an inverse relationship between deliberation time and grey-matter density, with alcoholics displaying slower choices related to grey-matter atrophy in key nodes of the motor control network. In particular, grey-matter density in the supplementary motor area, reduced in alcoholic patients, explained a significant amount of variability in their increased deliberation time. Tract-based spatial statistics revealed a significant relationship between CGT deliberation time and all white-matter indices, involving the most relevant commissural, projection and associative tracts. The lack of choice impairments other than increased deliberation time highlights reduced processing speed, mediated both by grey-matter and white-matter alterations, as a possible marker of a generalized executive impairment extending to the output stages of decision-making. These results pave the way to further studies aiming to tailor novel rehabilitation strategies and assess their functional outcomes.

The development of alcohol habits is considered a form of maladaptive reinforced learning, with sustained alcohol use resulting in the strengthening of associative links between consumption and either rewarding, or the lack of aversive, experiences. Despite recent efforts in characterizing decision-making skills in alcohol-use-disorder (AUD), it is still unknown whether impaired behavioural learning in AUD patients reflects a defective processing and anticipation of choice-related, cognitively mediated, emotions such as regret or relief for what might have been under a different choice. We administered a Wheel-of-Fortune (WoF) task to 26 AUD patients and 19 healthy controls, to investigate possible alterations in adjusting choices to the magnitude of experienced regret/relief, and in other facets of decision-making performance such as choice latency. AUD patients displayed both longer deliberation time than healthy controls, and impaired adaptations to previous outcome-related negative emotions. Although further evidence is needed to unveil the cognitive mechanisms underlying AUD patients’ abnormal choice, the present results highlight important implications for the clinical practice, e.g. in terms of cognitive treatments aiming to shape faulty perceptions about negative emotions associated with excessive alcohol exposure.

The persistence of addictive behaviours despite their adverse consequences highlights decreased punishment sensitivity as a facet of decision-making impairments in Alcohol Use Disorder (AUD). This attitude departs from the typical loss aversion (LA) pattern, i.e. the stronger sensitivity to negative than positive outcomes, previously associated with striatal and limbic-somatosensory responsiveness in healthy individuals. Consistent evidence highlights decreased LA as a marker of disease severity in AUD, but its neural bases remain largely unexplored. AUD-specific modulations of frontolateral activity by LA were previously related to the higher executive demands of anticipating losses than gains, but the relationship between LA and executive/working-memory performance in AUD is debated. Building on previous evidence of overlapping neural bases of LA during decision-making and at rest, we investigated a possible neural signature of altered LA in AUDs, and its connections with executive skills, in terms of complementary facets of resting-state functioning. In patients, smaller LA than controls, unrelated to executive performance, reflected reduced connectivity within striatal and medial temporal networks, and altered connectivity from these regions to the insular-opercular cortex. AUD-specific loss-related modulations of intrinsic connectivity thus involved structures previously associated both with drug-seeking and with coding the trade-off between appetitive and aversive motivational drives. These findings fit the hypothesis that altered striatal coding of choice-related incentive value, and interoceptive responsiveness to prospective outcomes, enhance neural sensitivity to drug-related stimuli in addictions. LA and its neural bases might prove useful markers of AUD severity and effectiveness of rehabilitation strategies targeting the salience of negative choice outcomes.

Alcohol Use Disorder (AUD) entails chronic effects on brain structure. Neurodegeneration due to alcohol toxicity is a neural signature of executive impairment typically observed in AUD, previously related to both gray-matter volume/density and white-matter abnormalities. Recent studies highlighted the role of meso-cortico-limbic structures supporting the salience and executive networks, in which the extent of neurostructural damage is significantly related to patients’ executive performance. Here we aim to integrate multimodal information on gray-matter and white-matter features with a multivariate data-driven approach (joint Independent Component Analysis, jICA), and to assess the relationship between the extent of damage in the resulting neurostructural superordinate components and executive profile in AUD. Twenty-two AUD patients and 18 matched healthy controls (HC) underwent a Magnetic Resonance Imaging (MRI) protocol, alongside clinical and neuropsychological examinations. We ran jICA on five neurostructural features, including gray-matter density and different diffusion tensor imaging metrics. We extracted 12 Independent Components (ICs) and compared the resulting mixing coefficients in patients vs. HC. Finally, we correlated significant ICs with executive and clinical variables. One out of 12 ICs (IC11) discriminated patients from healthy controls and correlated positively both with executive performance in all subjects, and with lifetime duration of alcohol abuse in patients. In line with previous related evidence, this component involved widespread gray-matter and white-matter patterns including key nodes and fiber tracts of salience, default-mode and central executive networks. These findings highlighted the role of multivariate data integration as a valuable approach revealing superordinate hallmarks of neural changes related to cognition in neurological and psychiatric populations.

Previous inconsistencies on the effects of implicitly processing positively - vs. negatively - connotated emotional words might reflect the influence of uncontrolled psycholinguistic dimensions, and/or social facets inherent in putative "emotional" stimuli. Based on the relevance of social features in semantic cognition, we developed a socio-emotional Stroop task to assess the influence of social vs. individual (non-social) emotional content, besides negative vs. positive valence, on implicit word processing. The effect of these variables was evaluated in terms of performance and RTs, alongside associated brain activity/connectivity. We matched conditions for several psycholinguistic variables, and assessed a modulation of brain activity/connectivity by trial-wise RT, to characterize the maximum of condition- and subject-specific variability. RTs were tracked by insular and anterior cingulate activations likely reflecting implicit attention to stimuli, interfering with task-performance based on condition-specific processing of their subjective salience. Slower performance for negative than neutral/positive words was tracked by left-hemispheric structures processing negative stimuli and emotions, such as fronto-insular cortex, while the lack of specific activations for positively-connotated words supported their marginal facilitatory effect. The speeding/slowing effects of processing positive/negative individual emotional stimuli were enhanced by social words, reflecting in specific activations of the right anterior temporal and orbitofrontal cortex, respectively. RTs to social positive and negative words modulated connectivity from these regions to fronto-striatal and sensorimotor structures, respectively, likely promoting approach vs. avoidance dispositions shaping their facilitatory vs. inhibitory effect. These results might help assessing the neural correlates of impaired social cognition and emotional regulation, and the effects of rehabilitative interventions.

While the discussion on the foundations of social understanding mainly revolves around the notions of empathy, affective mentalizing, and cognitive mentalizing, their degree of overlap versus specificity is still unclear. We took a meta-analytic approach to unveil the neural bases of cognitive mentalizing, affective mentalizing, and empathy, both in healthy individuals and pathological conditions characterized by social deficits such as schizophrenia and autism. We observed partially overlapping networks for cognitive and affective mentalizing in the medial prefrontal, posterior cingulate, and lateral temporal cortex, while empathy mainly engaged fronto-insular, somatosensory, and anterior cingulate cortex. Adjacent process-specific regions in the posterior lateral temporal, ventrolateral, and dorsomedial prefrontal cortex might underpin a transition from abstract representations of cognitive mental states detached from sensory facets to emotionally-charged representations of affective mental states. Altered mentalizing-related activity involved distinct sectors of the posterior lateral temporal cortex in schizophrenia and autism, while only the latter group displayed abnormal empathy related activity in the amygdala. These data might inform the design of rehabilitative treatments for social cognitive deficits.

We have previously shown that activity and connectivity within and between the action observation and mentalizing brain systems reflect the degree of positive dimensions expressed by social interactions such as cooperativity and affectivity, respectively. Here we aim to extend this evidence by investigating the neural bases of processing negative dimensions of observed interactions, such as competition and affective conflict, possibly representing a benchmark for different pathological conditions. In this fMRI study 34 healthy participants were shown pictures depicting interactions characterized by two crossed dimensions, i.e. positively- vs. negatively- connotated social intentions mainly expressed in terms of motor acts vs. mental states, i.e. cooperative, competitive, affective and conflicting interactions. We confirmed the involvement of the action observation and mentalizing networks in processing intentions mainly expressed through motor acts (cooperative/competitive) vs. mental states (affective/conflicting), respectively. Results highlighted the selective role of the left pSTS/TPJ in decoding social interactions, even when compared with parallel actions by non-interacting individuals. Its right-hemispheric homologue displayed stronger responses to negative than positive social intentions, regardless of their motor/mental status, and decreased connectivity with the medial prefrontal cortex (mPFC) when processing negative interactions. The resulting mPFC downregulation by negative social scenes might reflect an adaptive response to socio-affective threats, via decreased mentalizing when facing negative social stimuli. This evidence on the brain mechanisms underlying the decoding of real complex interactions represents a baseline for assessing both the neural correlates of impaired social cognition, and the effects of rehabilitative treatments, in neuro-psychiatric diseases or borderline conditions such as loneliness.

The neural bases of cognitive impairment(s) in alcohol use disorders (AUDs) might reflect either a global brain damage underlying different neuro-cognitive alterations, or the involvement of specific regions mostly affected by alcohol neuro-toxic effects. While voxel-based-morphometry (VBM) studies have shown a distributed atrophic pattern in fronto-limbic and cerebellar structures, the lack of comprehensive neuro-cognitive assessments prevents previous studies from drawing robust inferences on the specificity of the association between neuro-structural and cognitive impairments in AUDs. To fill this gap, we addressed the neuro-structural bases of cognitive impairment in AUDs, by coupling VBM with an in-depth neuropsychological assessment. VBM results highlighted a diffuse pattern of grey matter reduction in patients, involving the key-nodes of the meso-cortico-limbic (striatum, hippocampus, medial prefrontal cortex), salience (insular and dorsal anterior cingulate cortex) and executive (inferior frontal cortex) networks. Grey matter density in the insular and anterior cingulate sectors of the salience network, significantly decreased in patients, explained almost half of variability in their defective attentional and working-memory performance. The multiple cognitive and neurological impairments observed in AUDs might thus reflect a specific executive deficit associated with the selective damage of a salience-based neural mechanism enhancing access to cognitive resources required for controlled cognition and behaviour

Alcohol Use Disorders (AUD) is associated with negative consequences on global functioning, likely reflecting chronic changes in brain morphology and connectivity. Previous attempts to characterize cognitive impairment in AUD addressed patients’ performance in single domains, without considering their cognitive profile as a whole. While altered cognitive performance likely reflects abnormal white-matter microstructural properties, to date no study has directly addressed the relationship between a proxy of patients’ cognitive profile and microstructural damage. To fill this gap we aimed to characterize the microstructural damage pattern, and its relationship with cognitive profile, in treatment-seeking AUD patients. Twenty-two AUD patients and 18 healthy controls underwent a multimodal MRI protocol including diffusion tensor imaging (DTI), alongside a comprehensive neurocognitive assessment. We used a principal component analysis (PCA) to identify superordinate components maximally explaining variability in cognitive performance, and whole-brain voxelwise analyses to unveil the neural correlates of AUD patients’ cognitive impairment in terms of different white-matter microstructural features, i.e. fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD). PCA revealed a basic executive component, significantly impaired in AUD patients, associated with tasks tapping visuo-motor processing speed, attention and working-memory. Within a widespread pattern of white-matter damage in patients, we found diverse types of relationship linking WM microstructure and executive performance: (i) in the whole sample, we observed a linear relationship involving MD/RD metrics within both ‘superficial’ white-matter systems mediating connectivity within large-scale brain networks, and deeper systems modulating their reciprocal connections; (ii) in AUD patients vs. controls, a performance-by-group interaction highlighted a MD/AD pattern involvi

The neural bases of cognitive impairment(s) in alcohol use disorders (AUDs) have been explained either with the specific involvement of frontal regions mostly affected by alcohol neurotoxic effects, or with a global brain damage underlying different neuro-cognitive alterations. Novel insights into this issue might come from the analysis of resting-state brain activity, representing a baseline level of intrinsic connectivity within and between the networks underlying cognitive performance. We thus addressed the neural bases of cognitive impairment(s) in 22 AUD patients, compared with 18 healthy controls, by coupling resting-state fMRI with an in-depth neuropsychological assessment of the main cognitive domains. We assessed a relationship between AUD patients' cognitive impairment and two complementary facets of intrinsic brain functioning, i.e., intensity of activation and functional network connectivity, related to the strength of connectivity within and between resting-state networks, respectively. Alcoholic patients' decreased cognitive performance involved specifically an executive domain associated with attentional and working-memory tasks. This impairment reflected an abnormal relationship, in patients versus controls, between cognitive performance and the intensity of intrinsic activity in the dorsolateral prefrontal and striatal nodes of the executive control network. Functional connectivity between the same structures was positively correlated with executive performance in the whole sample, but significantly reduced in patients. The present data suggest that AUD patients' executive impairment reflects dysfunctional connectivity between the cortical and subcortical nodes of the networks underlying cognitive control on goal-directed behavior. This evidence provides a baseline for future studies addressing the abnormal neural architecture underlying cognitive impairment in AUDs and the outcome of rehabilitative treatment.

Neuroeconomics is providing insights into the neural bases of decision-making in normal and pathological conditions. In the neuropsychiatric domain, this discipline investigates how abnormal functioning of neural systems associated with reward processing and cognitive control promotes different disorders, and whether such evidence may inform treatments. This endeavor is crucial when studying different types of addiction, which share a core promoting mechanism in the imbalance between impulsive subcortical neural signals associated with immediate pleasurable outcomes and inhibitory signals mediated by a prefrontal reflective system. The resulting impairment in behavioral control represents a hallmark of alcohol use disorders (AUDs), a chronic relapsing disorder characterized by excessive alcohol consumption despite devastating consequences. This review aims to summarize available magnetic resonance imaging (MRI) evidence on reward-related decision-making alterations in AUDs, and to envision possible future research directions. We review functional MRI (fMRI) studies using tasks involving monetary rewards, as well as MRI studies relating decision-making parameters to neurostructural gray- or white-matter metrics. The available data suggest that excessive alcohol exposure affects neural signaling within brain networks underlying adaptive behavioral learning via the implementation of prediction errors. Namely, weaker ventromedial prefrontal cortex activity and altered connectivity between ventral striatum and dorsolateral prefrontal cortex likely underpin a shift from goal-directed to habitual actions which, in turn, might underpin compulsive alcohol consumption and relapsing episodes despite adverse consequences. Overall, these data highlight abnormal fronto-striatal connectivity as a candidate neurobiological marker of impaired choice in AUDs. Further studies are needed, however, to unveil its implications in the multiple facets of decision-making.

Decoding the meaning of others’ actions, a crucial step for social cognition, involves different neural mechanisms. While the “mirror” and “mentalizing” systems have been associated with, respectively, the processing of biological actions versus more abstract information, their respective contribution to intention understanding is debated. Processing social interactions seems to recruit both neural systems, with a different weight depending on cues emphasizing either shared action goals or shared mental states. We have previously shown that observing cooperative and affective social interactions elicits stronger activity in key nodes of, respectively, the mirror (left posterior superior temporal sulcus (pSTS), superior parietal cortex (SPL), and ventral/dorsal premotor cortex (vPMC/dPMC)) and mentalizing (ventromedial prefrontal cortex (vmPFC)) systems. To unveil their causal organization, we investigated the effective connectivity underlying the observation of human social interactions expressing increasing cooperativity (involving left pSTS, SPL, and vPMC) versus affectivity (vmPFC) via dynamic causal modeling in 36 healthy human subjects. We found strong evidence for a model including the pSTS and vPMC as input nodes for the observed interactions. The extrinsic connectivity of this model undergoes oppositely valenced modulations, with cooperativity promoting positive modulations of connectivity between pSTS and both SPL (forward) and vPMC (mainly backward), and affectivity promoting reciprocal positive modulations of connectivity between pSTS and vmPFC (mainly backward). Alongside fMRI data, such divergent effective connectivity suggests that different dimensions underlying the processing of social interactions recruit distinct, although strongly interconnected, neural pathways associated with, respectively, the bottom–up visuomotor processing of motor intentions, and the top–down attribution of affective/mental states.

Decision making under risk entails the anticipation of prospective outcomes, typically leading to the greater sensitivity to losses than gains known as loss aversion. Previous studies on the neural bases of choice-outcome anticipation and loss aversion provided inconsistent results, showing either bidirectional mesolimbic responses of activation for gains and deactivation for losses, or a specific amygdala involvement in processing losses. Here we focused on loss aversion with the aim to address interindividual differences in the neural bases of choice-outcome anticipation. Fifty-six healthy human participants accepted or rejected 104 mixed gambles offering equal (50%) chances of gaining or losing different amounts of money while their brain activity was measured with functional magnetic resonance imaging (fMRI). We report both bidirectional and gain/loss-specific responses while evaluating risky gambles, with amygdala and posterior insula specifically tracking the magnitude of potential losses. At the individual level, loss aversion was reflected both in limbic fMRI responses and in gray matter volume in a structural amygdala-thalamus-striatum network, in which the volume of the "output" centromedial amygdala nuclei mediating avoidance behavior was negatively correlated with monetary performance. We conclude that outcome anticipation and ensuing loss aversion involve multiple neural systems, showing functional and structural individual variability directly related to the actual financial outcomes of choices. By supporting the simultaneous involvement of both appetitive and aversive processing in economic decision making, these results contribute to the interpretation of existing inconsistencies on the neural bases of anticipating choice outcomes.

Previous reports suggest that the internal organization of semantic memory is in terms of different "types of knowledge," including "sensory" (information about perceptual features), "action" (motor-based knowledge of object utilization), and "functional" (abstract properties, as function and context of use). Consistent with this view, a specific loss of action knowledge, with preserved functional knowledge, has been recently observed in patients with left frontoparietal lesions. The opposite pattern (impaired functional knowledge with preserved action knowledge) was reported in association with anterior inferotemporal lesions. In the present study, the cerebral representation of action and functional knowledge was investigated using event-related analysis of functional magnetic resonance imaging data. Fifteen subjects were presented with pictures showing pairs of manipulable objects and asked whether the objects within each pair were used with the same manipulation pattern ("action knowledge" condition) or in the same context ("functional knowledge" condition). Direct comparisons showed action knowledge, relative to functional knowledge, to activate a left frontoparietal network, comprising the intraparietal sulcus, the inferior parietal lobule, and the dorsal premotor cortex. The reverse comparison yielded activations in the retrosplenial and the lateral anterior inferotemporal cortex. These results confirm and extend previous neuropsychological data and support the hypothesis of the existence of different types of information processing in the internal organization of semantic memory.

Aspetti fiscali dell'economia digitale, sia ai fini delle imposte dirette, sia ai fini dell'iva

Decoding others' intentions is a crucial aspect of social cognition. Neuroimaging studies suggest that inferring immediate goals engages the neural system for action understanding (i.e. mirror system), while the decoding of long-term intentions requires the system subserving the attribution of mental states (i.e. mentalizing). A controversial issue, stimulated by recent inconsistent results, concerns whether the two systems are concurrently vs. exclusively involved in intention understanding. This issue is particularly relevant in the case of social interactions, whose processing has been mostly, but not uncontroversially, associated with the mentalizing system. We tested the alternative hypothesis that the relative contribution of the two systems in intention understanding may also depend on the shared goal of interacting agents. To this purpose, 27 participants observed social interactions differing in their cooperative vs. affective shared goal during functional-Magnetic-Resonance-Imaging. The processing of both types of interactions activated the right temporo-parietal junction involved in mentalizing on action goals. Additionally, whole-brain and regions-of-interest analyses showed that the action understanding system (inferior prefrontal-parietal cortex) was more strongly activated by cooperative interactions, while the mentalizing-proper system (medial prefrontal cortex) was more strongly engaged by affective interactions. These differences were modulated by individual differences in empathizing. Both systems can thus be involved in understanding social intentions, with a relative weighting depending on the specific shared goal of the interaction

The timing and neural processing of the understanding of social interactions was investigated by presenting scenes in which 2 people performed cooperative or affective actions. While the role of the human mirror neuron system (MNS) in understanding actions and intentions is widely accepted, little is known about the time course within which these aspects of visual information are automatically extracted. Event-Related Potentials were recorded in 35 university students perceiving 260 pictures of cooperative (e.g., 2 people dragging a box) or affective (e.g., 2 people smiling and holding hands) interactions. The action's goal was automatically discriminated at about 150-170 ms, as reflected by occipito/temporal N170 response. The swLORETA inverse solution revealed the strongest sources in the right posterior cingulate cortex (CC) for affective actions and in the right pSTS for cooperative actions. It was found a right hemispheric asymmetry that involved the fusiform gyrus (BA37), the posterior CC, and the medial frontal gyrus (BA10/11) for the processing of affective interactions, particularly in the 155-175 ms time window. In a later time window (200-250 ms) the processing of cooperative interactions activated the left post-central gyrus (BA3), the left parahippocampal gyrus, the left superior frontal gyrus (BA10), as well as the right premotor cortex (BA6). Women showed a greater response discriminative of the action's goal compared to men at P300 and anterior negativity level (220-500 ms). These findings might be related to a greater responsiveness of the female vs. male MNS. In addition, the discriminative effect was bilateral in women and was smaller and left-sided in men. Evidence was provided that perceptually similar social interactions are discriminated on the basis of the agents' intentions quite early in neural processing, differentially activating regions devoted to face/body/action coding, the limbic system and the MNS. © 2011 Proverbio et al.