Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease after Alzheimer’s disease, globally. Dopaminergic neuron degeneration in substantia nigra pars compacta and aggregation of misfolded alpha-synuclein are the PD hallmarks, accompanied by motor and non-motor symptoms. Several viruses have been linked to the appearance of a post-infection parkinsonian phenotype. Coronavirus disease 2019 (COVID-19), caused by emerging severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, has evolved from a novel pneumonia to a multifaceted syndrome with multiple clinical manifestations, among which neurological sequalae appear insidious and potentially long-lasting. Exosomes are extracellular nanovesicles bearing a complex cargo of active biomolecules and playing crucial roles in intercellular communication under pathophysiological conditions. Exosomes constitute a reliable route for misfolded protein transmission, contributing to PD pathogenesis and diagnosis. Herein, we summarize recent evidence suggesting that SARS-CoV-2 infection shares numerous clinical manifestations and inflammatory and molecular pathways with PD. We carry on hypothesizing that these similarities may be reflected in exosomal cargo modulated by the virus in correlation with disease severity. Travelling from the periphery to the brain, SARS-CoV-2-related exosomal cargo contains SARS-CoV-2 RNA, viral proteins, inflammatory mediators, and modified host proteins that could operate as promoters of neurodegenerative and neuroinflammatory cascades, potentially leading to a future parkinsonism and PD development.

Long-post-coronavirus disease-2019 (COVID-19) patients tend to claim residual symptomatology from various systems, most importantly the respiratory and central nervous systems. Breathlessness and brain fog are the main complaints. The pulmonary function pattern is consistent with restrictive defects, which, in most cases, are self-resolved, while the cognitive profile may be impaired. Rehabilitation is an ongoing field for holistic management of long-post-COVID-19 patients. Virtual reality (VR) applications may represent an innovative implementation of rehabilitation. We aimed to investigate the effect of exercise with and without the VR system and to assess further breathlessness and functional fitness indicators in long-post-COVID-19 patients with mild cognitive impairment after self-selected exercise duration using the VR system. Twenty long-post-COVID-19 patients were enrolled in our study (age: 53.9 ± 9.1 years, male: 80%, body mass index: 28.1 ± 3.1 kg/m2). Participants' anthropometric data were recorded, and they underwent pulmonary functional test evaluation as well as sleep quality and cognitive assessment. The participants randomly exercised with and without a VR system (VR vs. no-VR) and, later, self-selected the exercise duration using the VR system. The results showed that exercise with VR resulted in a lower dyspnea score than exercise without VR. In conclusion, VR applications seem to be an attractive and safe tool for implementing rehabilitation. They can enhance performance during exercise and benefit patients with both respiratory and cognitive symptoms.

Background The aim of our study was to investigate the prevalence and associations of cognitive impairment in COVID‐19 survivors in the post‐acute setting. Method Our study is conducted in three post‐COVID‐19 outpatient clinics in tertiary hospitals in Greece. Eligible subjects included previously hospitalized COVID‐19 survivors with mild to moderate disease, returning for follow‐up at least two months post‐discharge. Exclusion criteria included intensive care unit admission, intubation, a history of neurodegenerative disease and other significant comorbidities. Study measurements included demographics, clinical evaluation, medical, family history, anthropometrics, 6‐minute walk test (6MWT), 30 seconds sit‐to‐stand (30STS), handgrip strength, spirometry, Pittsburgh Sleep Quality Index (PSQI), the Montreal Cognitive Assessment (MoCA), reactive oxygen metabolites (dROMs) and plasma antioxidant capacity (PAT). Cognitive impairment was considered on MoCA ≤24. Result 142 COVID‐19 survivors were included in the study (110 Male, 32 Female; Mean age of 56.16±10.92). A total of 47.2% presented with cognitive decline (CD) as indicated by a MoCA score ≤24. Cognitive decline prevalence by SARS‐CoV‐2 variant of concern (VOC) was 39.5%, 50% and 62.5% for Alpha, Beta and Delta, correspondingly. A binary logistic regression model controlling for age, gender and VOC indicated that the diffusing capacity for carbon monoxide (DLCO) was independently associated with MoCA ≤24 (p = 0.014, OR = 0.669, 95%CI: 0.484‐0.923). Compared to severe untreated OSAS (n = 28), distinct domains but similar prevalence of cognitive impairment was noted. Conclusion Diffusion capacity abnormalities for carbon monoxide in COVID‐19 survivors as noted in other studies, may be implicated in the development of cognitive impairment.