BACKGROUND Physical activity (PA) is essential for individuals with Parkinson's disease (PD) to maintain functional independence and quality of life. However, difficulties in accurately measuring PA complicate the identification of effective and beneficial interventions. Understanding the discrepancies between self-reported and objectively measured PA is critical for clinical practice. This study compared self-reported and objectively measured PA among people with PD, considering their participation in functional physical rehabilitation (FPR). MATERIAL AND METHODS The International Physical Activity Questionnaire and Actigraph GT3X+ were used to measure PA. Patients with PD (n=47) in stages II or III of the disease according to the Hoehn and Yahr scale, aged 64.37±7.12 years, with disease duration of 6.29±4.02 years were divided into 2 groups: participating (Group A) and not participating (Group B) in FPR. The FPR program combined motor symptom-targeted therapy with task-oriented training to improve functional independence and quality of life. RESULTS Comparing self-reported weekly PA with the objective showed statistically significant differences (P<0.05) in both groups - the self-reported PA was 8.61% higher in Group A and 56.70% higher in Group B. In Group A, declared PA was higher than the objective in all intensity zones: by 19.50% in high, by 10.52% in moderate, and by 7.35% in low. In Group B, declared PA was higher than the objective by 250% in high-intensity, by 90.66% in moderate-intensity, and by 48.32% in low-intensity. CONCLUSIONS We found significant differences between self-reported and objectively measured PA in people with PD, based on their participation in FPR. Participation in FPR seems to improve the accuracy of PA self-assessment, demonstrating the importance of objective PA measurement in clinical practice.

Drug-induced parkinsonism (DIP) is the second most common cause of parkinsonian syndromes after idiopathic Parkinson’s disease (iPD), accounting for approximately 15-25% of cases in older adults. While DIP typically results from antipsychotic-induced dopamine receptor blockade and is often reversible, iPD is a progressive neurodegenerative disorder characterized by asymmetrical onset, resting tremor, and good response to levodopa. Distinguishing between these conditions is clinically important but often challenging. The aim of this article is to discuss the diagnostic and therapeutic challenges involved in differentiating DIP from iPD in patients with psychiatric disorders who are chronically treated with antipsychotics. Based on the case of a 52-year-old man with a long-standing history of schizophrenia treatment, the diagnostic process and clinical manifestations leading to the final diagnosis are presented. The patient developed Parkinsonian symptoms during olanzapine therapy, initially suggesting DIP. This paper discusses the clinical indicators differentiating DIP from iPD, as well as the critical role of single photon emission computed tomography (SPECT) with ioflupane-123 (DaTSCAN) in the differential diagnosis of Parkinsonism in selected, ambiguous cases. The described case illustrates the phenomenon of so-called "unmasked Parkinson’s disease" and highlights the need for detailed neurological monitoring in patients suspected of having DIP. It is essential to consider iPD as an independent cause of movement disorders in patients treated with antipsychotics. Early diagnosis and appropriate treatment of the underlying cause of Parkinsonism can significantly reduce extrapyramidal symptoms and improve the patient’s quality of life.

Introduction and objective: Although recent findings reveal potential contributing factors to Parkinson’s disease, ongoing research remains essential to further understand and substantiate these connections, identifying lifestyle patterns and biopsychological factors that may contribute to either the onset or prevention of Parkinson’s disease. Materials and methods: This study analyses the interactions among genetics, neuroplasticity, interoception, mindfulness, lifestyle, environment, and Parkinson’s disease, facilitating exploration of the underlying choices that influence disease development. While mediated factors do not directly cause Parkinson’s disease, they affect symptom severity, disease progression, and overall quality of life. With these insights, based on comparative observation and the application of a thought experiment, a Collaborative Impact Model was developed to enhance knowledge of contributing factors to Parkinson’s disease. The study had no human subjects. Results: Observations suggest that genetics and neuroplasticity, significantly shaped by lifestyle, directly influence the onset and progression of Parkinson’s disease. Genetic predispositions and adaptive neuroplasticity determine neural resilience or vulnerability, while environmental factors, interoception, mindfulness, and general lifestyle indirectly influence Parkinson’s disease by modulating stress, inflammation, cognitive health, and emotional regulation, thus affecting overall disease trajectory and symptom severity. Conclusions: The outlined approach captures the complex interplay between genetic factors, neuroplastic adaptation, and external influences, emphasising how lifestyle choices can have both immediate and long-term effects. It facilitates a multidimensional strategy for prevention, management, patient support, and education in Parkinson’s disease.

Background/objective: Endovascular thrombectomy (EVT) is the standard treatment for acute ischemic stroke due to large-vessel occlusion (LVO), but its impact on cognition is less clearly defined despite the high prevalence of post-stroke cognitive impairment. We systematically reviewed randomized controlled trials and observational studies reporting objectively measured cognitive outcomes after EVT in adults with acute ischemic stroke. Methods: Following PRISMA 2020, a systematic search of PubMed, Embase, the Cochrane Library, and Scopus was conducted between 1 March and 31 October 2025 for studies published from 1 January 2015 to 31 October 2025. Eligible studies reported objectively measured post-stroke cognitive outcomes after EVT, with or without intravenous thrombolysis (IVT). Due to substantial heterogeneity in cognitive assessment tools, outcome definitions, and follow-up time points, quantitative pooling was not feasible and results were therefore synthesized narratively. Results: Twenty-three studies (∼3,300 participants; 3 RCTs, 20 observational) met the inclusion criteria. Across most comparative studies, EVT was associated with better cognitive outcomes than IVT or best medical therapy, typically yielding on average 1–4 point higher scores on the Montreal Cognitive Assessment (MoCA) or Mini-Mental State Examination (MMSE) at early to mid-term follow-up. The most consistent benefits were observed in executive functions, with more variable but favorable effects on memory. Worse cognitive outcomes were linked to larger infarct volume, combined gray–white matter involvement, territorial infarct patterns, and longer time to reperfusion. Exploratory proteomic work suggested associations between inflammatory and neurotrophic markers and cognitive recovery. Despite these benefits, post-stroke cognitive impairment remained frequent. Conclusion: Endovascular thrombectomy, particularly when performed rapidly with successful reperfusion, is associated with more favorable cognitive outcomes, especially in global cognition and executive function. However, persistent cognitive deficits remain common, highlighting the need for standardized cognitive assessment and longer-term follow-up in future EVT studies. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251156363 , identifier CRD420251156363.

Alzheimer’s Disease (AD) is a progressive neurodegenerative brain disorder, the prevalence of which increases rapidly with the aging population. The pathogenesis of AD is based on the accumulation of β-amyloid and tau protein, leading to progressive neuronal loss, synaptic dysfunction, and dementia. Modern diagnostic approaches focus on identifying disease biomarkers that enable their detection even before clinical symptoms appear. Simultaneously, intensive research on biological therapies has led to significant discoveries in the treatment of AD. Monoclonal antibodies, such as aducanumab, lec-anemab, and donanemab, have demonstrated the ability to reduce amyloid plaques in the brain; however, the clinical effects observed lag behind the magnitude of biomarker changes, and their impact on cognitive function remains a subject of debate. Additionally, therapies targeting tau protein, as well as new strategies like antisense oligonucleotides and immunotherapies, open new perspectives in the treatment of AD. Promising are also targeted therapies focused on microglial modulation and modern technologies for drug delivery across the blood-brain barrier. This article is a narrative literature review based on a search of the MEDLINE (via PubMed) and SCOPUS databases for the years 2018– 2025, and incorporates the latest research and future perspectives on the diagnosis and treatment of Alzheimer’s disease.