Blood uric acid represents an important biomarker in sporadic Parkinson's disease (PD). Whether uric acid levels change in genetic forms of PD is beginning to be assessed. The aim of the present study was to evaluate differences in serum uric acid level among PD patients harboring mutations in the glucocerebrosidase (GBA1) gene, sporadic PD, and healthy controls followed longitudinally. Longitudinal 2-year serum uric acid measurement data of 120 GBA-PD patients have been downloaded from the Parkinson's Progression Markers Initiative (PPMI) database. This cohort was compared with 369 de novo sporadic PD patients and 195 healthy controls enrolled in the same study. Following adjustment for age, sex and BMI the GBA-PD cohort exhibited lower 2-year longitudinal uric acid level as compared to the controls (p = 0.016). Baseline uric acid measurements showed only a marginal difference (p = 0.119), but year 2 uric acid levels were lower in the GBA-PD cohort (p < 0.001). There was no difference in baseline, year 2 and 2-year longitudinal serum uric acid in the GBA-PD cohort as compared to sporadic PD (p = 0.664, p = 0.117 and p = 0.315). This is the first study to assess serum uric acid in a GBA-PD cohort. Our findings suggest that low serum uric acid might be a progression biomarker in GBA-PD. However, more studies (ideally longitudinal) on the association between low serum uric acid and clinical data in GBA-PD are needed. These results are consistent with data from previous reports assessing uric acid as a biomarker in other genetic forms of PD.

Education, training, and professional issues of radiographers in six European countries: a comparative review

Introduction: Previous epidemiological evidence has established the co-occurrence of malignant melanoma (MM) and Parkinson’s disease (PD). Shared molecular mechanisms have been proposed to be implicated in this relationship. The aim of the present study was to assess the prevalence of MM in patients with sporadic and genetic types of PD, as well as in asymptomatic carriers of PD-related genes. Methods: Data regarding past medical history and concomitant disease of 1416 patients with PD (including 20 participants with prodromal disease who phenoconverted to PD), 275 healthy controls (HCs) and 670 asymptomatic carriers of PD-related genes were obtained from the database of the Parkinson’s Progression Markers Initiative (PPMI). Focus was placed on information about a medical record of MM. We also retrieved data regarding the genetic status of selected PPMI participants with a positive MM history. Results: In total, 46 patients with PD reported a positive MM history. Concerning the genetic forms of PD, nine of these PD patients (2.47%) carried a Leucine Rich Repeat Kinase 2 (LRRK2) gene mutation (mainly the G2019S), while eight (4.49%) harbored a Glucocerebrosidase (GBA) gene mutation (mainly the N370S). No alpha-synuclein (SNCA) gene mutation was identified in patients with an MM history. The remaining 29 PD patients (3.5%) were genetically undetermined. In total, 18 asymptomatic carriers of PD-related genes had a positive medical history for MM: among them, 10 carried an LRRK2 gene mutation (2.69%) and 10 a GBA gene mutation (3.51%) (2 were dual carriers). MM history was identified for seven HCs (2.5%). Conclusions: We replicated the previously reported association between genetically undetermined PD (GU-PD) and MM. A correlation of LRRK2 mutations with the development of MM could not be verified in either symptomatic PD patients or asymptomatic carriers, implicating distinct pathogenetic mechanisms as compared to GU-PD. Importantly, despite the limited literature evidence on Gaucher disease, this study highlights for the first time the relatively high prevalence of MM among asymptomatic and symptomatic PD GBA mutation carriers, with potential clinical implications.

Cardiovascular disease (CVD) remains Europe’s leading cause of mortality, responsible for >45% of deaths. Beyond established risk factors (hypertension, diabetes, dyslipidaemia, smoking, obesity), psychosocial elements—depression, anxiety, financial stress, personality traits, and trauma—significantly influence CVD development and progression. Behavioural Cardiology addresses this connection by systematically incorporating psychosocial factors into prevention and rehabilitation protocols. This review examines the HEARTBEAT model, developed by Greece’s first Behavioural Cardiology Unit, which aligns with current European guidelines. The model serves dual purposes: primary prevention (targeting at-risk individuals) and secondary prevention (treating established CVD patients). It is a personalised medicine approach that integrates psychosocial profiling with traditional risk assessment, utilising tailored evaluation tools, caregiver input, and multidisciplinary collaboration to address personality traits, emotional states, socioeconomic circumstances, and cultural contexts. The model emphasises three critical implementation aspects: (1) digital health integration, (2) cost-effectiveness analysis, and (3) healthcare system adaptability. Compared to international approaches, it highlights research gaps in psychosocial interventions and advocates for culturally sensitive adaptations, particularly in resource-limited settings. Special consideration is given to older populations requiring tailored care strategies. Ultimately, Behavioural Cardiology represents a transformative systems-based approach bridging psychology, lifestyle medicine, and cardiovascular treatment. This integration may prove pivotal for optimising chronic disease management through personalised interventions that address both biological and psychosocial determinants of cardiovascular health.