Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has been discussed in the context of Parkinson’s disease (PD) over the last three years. Now that we are entering the long-term phase of this pandemic, we are intrigued to look back and see how and why the community of patients with PD was impacted and what knowledge we have collected so far. The relationship between COVID-19 and PD is likely multifactorial in nature. Similar to other systemic infections, a probable worsening of PD symptoms secondary to COVID-19, either transient or persistent (long COVID), has been demonstrated, while the COVID-19-related mortality of PD patients may be increased compared to the general population. These observations could be attributed to direct or indirect damage from SARS-CoV-2 in the central nervous system (CNS) or could result from general infection-related parameters (e.g., hospitalization or drugs) and the sequelae of the COVID-19 pandemic (e.g., quarantine). A growing number of cases of new-onset parkinsonism or PD following SARS-CoV-2 infection have been reported, either closely (post-infectious) or remotely (para-infectious) after a COVID-19 diagnosis, although such a link remains hypothetical. The pathophysiological substrate of these phenomena remains elusive; however, research studies, particularly pathology studies, have suggested various COVID-19-induced degenerative changes with potential associations with PD/parkinsonism. We review the literature to date for answers considering the relationship between SARS-CoV-2 infection and PD/parkinsonism, examining pathophysiology, clinical manifestations, vaccination, and future directions.

The present study aimed at exploring the association between eveningness and lifestyle-related variables, that is, body mass index, alcohol, and cigarette consumption, in adults (18-40years), focusing on the possible moderator effect of age and the role of sleep disturbances and circadian misalignment (social jetlag). A web-based survey was administered to 437 participants, covering demographics, lifestyle-related variables, chronotype, sleep quality, and daytime sleepiness. A subset of 206 participants wore a wrist actigraph for a week, allowing the creation of a sleep health index within the RU-SATED framework. Regression analysis was used to investigate the associations between chronotype and lifestyle-related outcomes, accounting for social jetlag and sleep health; and to explore the lifestyle trajectories over time. Evening chronotypes showed higher body mass index levels, consumed more alcohol, and smoked more cigarettes than other circadian typologies, in particular after 25 years of age. Poor sleep health and social jetlag significantly contribute to explaining evening types smoking behavior, while not affecting body mass index levels. Social jetlag plays a more important role compared to sleep disturbances and eveningness in predicting more detrimental drinking and smoking behavior. Participants who maintain the evening trait past the age of 25years are more prone to adopt an unhealthy lifestyle, especially if experiencing poor sleep health and circadian misalignment. Circadian preferences and sleep health should be considered when planning interventions aimed at promoting healthy lifestyles in adults aged 18-40years. Further investigations should explore the effect of modifications in lifestyle in the prevention of noncommunicable diseases.