Parkinson’s disease (PD) has become the second most common neurodegenerative condition following Alzheimer’s disease (AD), exhibiting high prevalence and incident rates. Current care strategies for PD patients include brief appointments, which are sparsely allocated, at outpatient clinics, where, in the best case scenario, expert neurologists evaluate disease progression using established rating scales and patient-reported questionnaires, which have interpretability issues and are subject to recall bias. In this context, artificial-intelligence-driven telehealth solutions, such as wearable devices, have the potential to improve patient care and support physicians to manage PD more effectively by monitoring patients in their familiar environment in an objective manner. In this study, we evaluate the validity of in-office clinical assessment using the MDS-UPDRS rating scale compared to home monitoring. Elaborating the results for 20 patients with Parkinson’s disease, we observed moderate to strong correlations for most symptoms (bradykinesia, rest tremor, gait impairment, and freezing of gait), as well as for fluctuating conditions (dyskinesia and OFF). In addition, we identified for the first time the existence of an index capable of remotely measuring patients’ quality of life. In summary, an in-office examination is only partially representative of most PD symptoms and cannot accurately capture daytime fluctuations and patients’ quality of life.

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, yet its underlying causes remain elusive. The conventional perspective on disease pathogenesis attributes alterations in neuronal excitability to molecular changes resulting in synaptic dysfunction. Early hyperexcitability is succeeded by a progressive cessation of electrical activity in neurons, with amyloid beta (Aβ) oligomers and tau protein hyperphosphorylation identified as the initial events leading to hyperactivity. In addition to these key proteins, voltage-gated sodium and potassium channels play a decisive role in the altered electrical properties of neurons in AD. Impaired synaptic function and reduced neuronal plasticity contribute to a vicious cycle, resulting in a reduction in the number of synapses and synaptic proteins, impacting their transportation inside the neuron. An understanding of these neurophysiological alterations, combined with abnormalities in the morphology of brain cells, emerges as a crucial avenue for new treatment investigations. This review aims to delve into the detailed exploration of electrical neuronal alterations observed in different AD models affecting single neurons and neuronal networks.

Psoriatic arthritis (PsA) is an inflammatory form of arthritis that belongs to the family of spondyloarthritis (SpA) and is related to skin psoriasis. The incidence and prevalence of the disease vary considerably between countries. PsA is classified into axial PsA and peripheral PsA, with a wide range of other extra-articular manifestations. Although the aetiology of the disease is unknown, genetic, environmental, and immunologic factors appear to affect its appearance. In recent years, the role of the immune system in the pathogenesis of PsA has been increasingly investigated. Specific cytokines such as tumour necrosis factor (TNF), interleukin (IL-) 17 and IL-23, play an essential role affecting joint structures. This observation led to the emergence of tumour necrosis factor inhibitors (TNFi) that offer considerable therapeutic benefit to PsA patients. However, chronic inflammation causes bone loss, while new bone formation may also occur in both peripheral and axial skeleton. The molecular mechanisms underlying these processes have not yet been fully understood. So far, the role of the Wnt/β-catenin pathway and its inhibitors (Dickkopf and sclerostin) has been evaluated in ankylosing spondylitis (AS), but in PsA has not been studied sufficiently. The present study aims to investigate the epidemiological characteristics and clinical features (articular and extra-articular manifestations) as well as the treatment of PsA patients in the region of northwestern (NW) Greece. It also aims to evaluate the role of specific cytokines and sclerostin in patients with PsA, giving evidence to possible future biomarkers or even therapeutic targets for the disease.

The role of oxidative stress in chronic pathological conditions of the nervous system is well-established, contributing to neuronal dysfunction and cell death. Numerous studies have sought pharmacologic agents with antioxidant effects for neurons, with controversial results. Our study aims to establish a valid and reproducible in vitro oxidative stress model in neurons, simulating initial stages of neurodegenerative disorders, focusing on morphological alterations in the dendritic field of neurons. Primary hippocampal cells from newborn rat brains were cultured for two weeks, and subsequently, different concentrations of hydrogen peroxide (H₂O₂) were applied for 24 h in cultures. Cell viability assays and flow cytometry were carried out to measure H₂O₂ effects on apoptosis, necrosis, and reactive oxygen species production. Finally, morphometric evaluation of the neuronal dendritic field was conducted, focused on dendritic length, branching, and spine density, with ImageJ software following immunostaining of neurons. Administration of 100 μΜ H₂O₂ for 24 h in primary hippocampal cultures resulted in significant alterations in dendritic morphology (one-way ANOVA, p < 0.05), without significantly affecting cell viability. These results demonstrate the impact of H₂O₂ on neuronal morphology and suggest that dendritic and spinal alterations could serve as sensitive markers of mild oxidative stress on neurons, prior to the activation of apoptotic mechanisms. This can be used as a surrogate model for the initial stages of neurodegenerative disorders when synaptic loss takes place, facilitating study of agent effectiveness with antioxidant therapeutic potential.

Routine clinical evaluations offer limited insight into daily variability and disease progression in Parkinson's disease (PD). While wearable devices are increasingly used to improve patient monitoring, evidence of their effectiveness remains scarce. To assess the efficacy of integrating a telemonitoring system into standard clinical procedures, highlighting its role in enabling efficient, patient-centered treatment adjustments. Thirty-five PD patients were monitored for 6 months using a telemonitoring device alongside standard care. Disease progression was assessed via MDS-UPDRS part III (UPDRS-p3) and device-reported outcomes (dUPDRS) at baseline and follow-up. Physicians provided feedback on telemedicine utility. UPDRS-p3 scores improved by 1.9-5.63 points. Changes in UPDRS-p3 strongly correlated with dUPDRS (r = 0.82). Sixty-two percent of patients had treatment modifications, 36% of which occurred remotely. Telemonitoring supported clinical decisions, detected subtle symptom changes, and offered valuable insights for improving motor symptoms and patient management.