ABSTRACT
Since the very beginning of the COVID-19 pandemic, numerous researchers have made an effort to determine the molecular composition of the SARS-CoV-2 virus, and the exact pathomechanism through which the virus exerts such a devastating effect on the host/infected organism. Recent scientific evidence highlights the affinity of the virus towards ACE2 receptors, which are widespread in multiple human systems, including the central nervous system (CNS) and cerebral vessels. Such an affinity may explain endothelial dysfunction and damage that is observed in COVID-positive patients in histopathological studies, with subsequent dysregulation of the cerebral circulation leading to transient or acute cerebrovascular accidents. In this paper, we aimed to evaluate the effects of COVID-related hypoxemia and direct viral invasion on the cerebral circulation, with special respect to the postulated pathomechanism, vulnerable groups of patients, clinical course and outcomes, as well as diagnostic imaging findings.
Subject(s)
Blood Coagulation Disorders , COVID-19 , Angiotensin-Converting Enzyme 2 , COVID-19/complications , Humans , Hypoxia , Pandemics , SARS-CoV-2ABSTRACT
In this review we attempt to collate the existing scientific evidence regarding the possible role of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the pathophysiology of Parkinson's disease (PD), as well as to investigate the impact of PD/parkinsonism on the clinical course of the viral infection itself. Since etiology of PD is not completely understood, various studies suggest different potential links between coronavirus disease 2019 (COVID-19) and PD. Suggested connections include, among others, similar prodromal symptoms, renin-angiotensin-aldosterone system involvement, or gut microbiome dysbiosis participation. Despite the initial assumptions that, as a mainly elderly population suffering from rigidity of respiratory muscles, impairment of cough reflex, and dyspnea, PD patients would be more susceptible to viral infection, and would experience a more aggressive course of COVID-19, the published scientific reports contain mutually exclusive data that require further investigation and meta-analysis.