Introduction: Empathy can be described as the ability to adopt another person’s perspective and comprehend, feel, share, and respond to their emotional experiences. Empathy plays an important role in these relationships and is constructed in human–robot interaction (HRI). This systematic review focuses on studies investigating human empathy toward robots. We intend to define empathy as the cognitive capacity of humans to perceive robots as equipped with emotional and psychological states.Methods: We conducted a systematic search of peer-reviewed articles using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched Scopus, PubMed, Web of Science, and Embase databases. All articles were reviewed based on the titles, abstracts, and full texts by two investigators (EM and CS) who independently performed data collection. The researchers read the full-text articles deemed suitable for the study, and in cases of disagreement regarding the inclusion and exclusion criteria, the final decision was made by a third researcher (VLB).Results: The electronic search identified 484 articles. After reading the full texts of the selected publications and applying the predefined inclusion criteria, we selected 11 articles that met our inclusion criteria. Robots that could identify and respond appropriately to the emotional states of humans seemed to evoke empathy. In addition, empathy tended to grow more when the robots exhibited anthropomorphic traits.Discussion: Humanoid robots can be programmed to understand and react to human emotions and simulate empathetic responses; however, they are not endowed with the same innate capacity for empathy as humans.

Background: Cognitive dysfunction is a common impairment observed in individuals with Multiple Sclerosis (MS), affecting key domains such as attention, information processing speed, memory, and executive functions. This deficit is typically identified through comprehensive neuropsychological assessments, which represent the gold standard for cognitive evaluation. In recent years, increasing efforts have been made to integrate neuropsychological findings with advanced neuroimaging techniques to better understand the neural substrates of cognitive dysfunction. Among these, Diffusion Tensor Imaging (DTI) has emerged as a valuable tool for investigating microstructural changes in white matter (WM) that may underlie cognitive deficits in MS. However, despite its clinical utility, the pathophysiological mechanisms contributing to cognitive impairment, particularly in subjects with Relapsing–Remitting MS (RRMS), remain complex and not yet fully understood. This review focuses on studies investigating WM alterations measured by DTI and their correlation with cognitive dysfunction as assessed through neuropsychological testing. Method: Papers were identified by searching in PubMed, Embase, Web of Science and Scopus databases from 2002 - the years, of first related published article, − to December 2024. From the initial 853, we included only 34 studies that met to eligibility criteria. Results: In subjects with RRMS, WM alterations, assessed through DTI, were found to correlate with cognitive dysfunction, as measured by standardized neuropsychological tests. These alterations were observed both in global WM and in specific regions, including the corpus callosum, thalamus, hippocampus, cerebellar structure, cingulum, and cerebral fascicles. Conclusion: These findings underscore the relevance of integrating neuropsychological assessment with advanced neuroimaging techniques, such as DTI, to enhance our understanding of cognitive impairment in RRMS. DTI-derived measures of WM integrity show promise as potential biomarkers of cognitive dysfunction, while cognitive profiling can help localize underlying neuropsychological damage. This integrated approach may improve early detection of cognitive alterations and support the development of targeted therapeutic strategies aimed at preserving cognitive functioning in individuals with MS. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251073195 , Identifier CRD420251073195.

Background and aims Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system, characterized by inflammation, demyelination, gliosis, and neuronal loss. Cognitive disorders are part of the clinical presentation, as well as in the early stages, with a prevalence rate ranging from 40 to 65% and are strictly associated with poor quality of life. In recent years, advances in the field of molecular biomarkers have contributed to improving the accuracy of cognitive diagnosis and to identifying subjects at risk of developing cognitive disorders. By focusing on longitudinal studies, this review aims to elucidate the temporal dynamics and potential predictive value of CSF and serum biomarkers in identifying cognitive decline and monitoring disease progression in MS. Methods A systematic review was conducted using the PRISMA guidelines. 827 studies were identified by searching PubMed, Scopus, and Web of Science between July and August 2025. After screening, 8 studies fulfilled the eligibility criteria and were included. Results NfL showed heterogeneous results: some studies identified it as a feasible biomarker able to predict cognitive decline, while others did not. GFAP did not show significant correlations. Parvalbumin was longitudinally associated with poorer cognition and greater fatigue. Specific microRNAs (miR-126.3p, miR-9p) were associated with processing speed decline. Higher BDNF levels were linked to cognitive improvement. Other biomarkers (OPN, IL-6, CHI3L1, CXCL13) provided insufficient evidence. Conclusions Findings add interesting contributions to the complex picture of the pathophysiology underpinning cognitive decline in MS. The most promising direction is the shift toward blood-based biomarkers, due to their minimally invasive nature and potential for clinical applicability, which may enable clinicians to anticipate, monitor, and potentially modify the cognitive trajectory of people living with MS.

Background: Group-based dance interventions (GBDIs) have emerged as a promising approach to rehabilitation for neurological disorders. This pilot study evaluated the feasibility and preliminary effects of a GBDI on motor function, cognition, fatigue, and quality of life in individuals with Relapsing–Remitting Multiple Sclerosis (RRMS). Methods: The intervention consisted of two 60-min ballet sessions per week over 10 weeks, structured as 10 min of warm-up, 40 min of ballet exercises, and 10 min of stretching. Assessments were conducted at baseline (T0) and post-intervention (T1). Concerning motor measures, balance was assessed using the Mini-BESTest; gait performance was evaluated through the 6-min walk test (6MWT), four square step test (FSST), and figure-of-8 walk test (F8WT); upper limb motor functions were assessed using the box and block test (BBT) and 9-hole peg test (9HPT). Regarding cognitive functions, the Rey auditory verbal learning test (RAVLT), symbol digit modalities test (SDMT), and trail making test A and B (TMT-A/B) were administered, while fatigue and quality of life were assessed using the modified fatigue impact scale (MFIS) and the Short Form survey-36 (SF-36), respectively. Results: At T1, participants improved in Mini-BESTest (+17.5%), 6MWT (+7.3%), and BBT dominant hand (+6.9%). Performance also improved on the following cognitive tests: RAVLT Immediate Recall (+5.9%), RAVLT Delayed Recall (+20.3%), SDMT (+47.4%), TMT-A (−21.2%), and (TMT-B −24.5%). Conclusions: The very small sample size (n = 4) and the lack of a control group probably restrict the generalizability of the findings. Consequently, the results obtained by this pilot study should be considered exploratory and hypothesis-generating rather than definitive evidence of a robust benefit. Future studies should confirm these findings by enlarging the intervention cohorts and adopting a randomized controlled design. In this sense, a 10-week GBDI may provide a solid base for a safe and promising dance-based rehabilitation program that could lead to improvements in motor, cognition, and psychosocial spheres in people with RRMS.

Apathy is a frequent and disabling non-motor symptom in Parkinson's disease (PD), characterized by diminished motivation, reduced goal-directed behavior, and emotional indifference. Growing evidence suggests that apathy in PD represents a distinct neuropsychiatric syndrome that may coexist with depression and global cognitive impairment, while also showing partially dissociable clinical and neural correlates. This systematic review aimed to investigate the neural substrates of apathy in PD by synthesizing evidence from structural and functional neuroimaging studies. Following PRISMA guidelines, we searched PubMed, Embase, Web of Science, and Scopus for studies assessing apathy in PD through neuroimaging techniques, including structural MRI, resting-state functional MRI, diffusion tensor imaging, PET/SPECT molecular imaging, and connectivity analyses. Apathy severity was evaluated using validated clinical scales, and findings were compared between PD population with and without apathy, as well as healthy controls. Across 16 heterogeneous studies, recurrent findings implicated structural, functional, and molecular alterations within fronto-striatal-limbic networks. However, differences in apathy measures and neuroimaging modalities limit direct comparability across studies and do not support a single unified imaging signature of apathy in PD. Apathetic PD subjects consistently exhibited reduced gray matter volume and altered spontaneous activity in the dorsolateral, inferior frontal gyri, anterior cingulate cortex (ACC), and nucleus accumbens, alongside disrupted functional and structural connectivity in fronto-limbic tracts. These alterations were significantly correlated with apathy severity and, in several studies, remained detectable after accounting for depressive symptoms or global cognitive status. Furthermore, the available findings suggest that apathy in PD may involve heterogeneous neurobiological mechanisms, including variable involvement of frontal, striatal, and limbic circuits; however, current evidence remains insufficient to support firm transmitter-based subtyping or treatment stratification. Current evidence suggests that apathy in PD involves partially dissociable neural correlates across prefrontal, striatal, and limbic systems. However, methodological heterogeneity across studies limits strong generalization, and future harmonized longitudinal studies are needed to clarify which findings are robust and clinically meaningful.

Background and aims Iron-related alterations are frequently implicated in multiple sclerosis (MS) neurodegeneration, but its relationship with clinical symptoms and cognitive impairment remains unclear. We systematically reviewed evidence linking iron-sensitive susceptibility-based magnetic resonance imaging (MRI) metrics to cognitive outcomes, in order to evaluate their potential role as diagnostic and prognostic biomarkers of cognitive decline in MS. Materials and methods A systematic review was conducted using the PRISMA guidelines. 600 studies were identified by searching PubMed, Scopus, Web of Science, and Embase in October 2025. After screening, 12 studies fulfilled the eligibility criteria and were included. Results Two main patterns emerged: (i) higher basal ganglia susceptibility/iron-related metrics are consistently linked to worse cognitive performance, particularly information processing speed and executive control; and (ii) thalamic findings are more variable in direction and clinical meaning, with susceptibility often capturing a mixed signal that overlaps with thalamic atrophy. Conclusions Iron-sensitive quantitative MRI captures clinically relevant deep gray matter (DGM) pathology associated with cognitive impairment in MS, with basal ganglia measures showing the strongest linkage with cognitive and clinical outcomes. Future studies should include harmonized methodology and a longitudinal component.