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Mol Neurobiol ; 58(9): 4477-4486, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1241710

ABSTRACT

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative agent of human COVID-19, not only causes flu-like symptoms and gut microbiome complications but a large number of infected individuals also experience a host of neurological symptoms including loss of smell and taste, seizures, difficulty concentrating, decreased alertness, and brain inflammation. Although SARS-CoV-2 infections are not more prevalent in Parkinson's disease patients, a higher mortality rate has been reported not only associated with older age and longer disease duration, but also through several mechanisms, such as interactions with the brain dopaminergic system and through systemic inflammatory responses. Indeed, a number of the neurological symptoms seen in COVID-19 patients, as well as the alterations in the gut microbiome, are also prevalent in patients with Parkinson's disease. Furthermore, biochemical pathways such as oxidative stress, inflammation, and protein aggregation have shared commonalities between Parkinson's disease and COVID-19 disease progression. In this review, we describe and compare the numerous similarities and intersections between neurodegeneration in Parkinson's disease and RNA viral infections, emphasizing the current SARS-CoV-2 global health crisis.


Subject(s)
COVID-19/physiopathology , Gastrointestinal Microbiome , Parkinson Disease/physiopathology , SARS-CoV-2 , Aged , COVID-19/complications , COVID-19/mortality , Cognition Disorders/etiology , Cytokines/physiology , Diet , Disease Progression , Dysbiosis/etiology , Dysbiosis/physiopathology , Humans , Inflammation , Metals, Heavy/toxicity , Models, Neurological , Nerve Degeneration , Olfactory Bulb/physiopathology , Olfactory Bulb/virology , Oxidative Stress , Parkinson Disease/etiology , Practice Guidelines as Topic , Protein Aggregation, Pathological/etiology , RNA Virus Infections/metabolism , RNA Virus Infections/physiopathology , Reactive Oxygen Species/metabolism , Sensation Disorders/etiology , alpha-Synuclein/metabolism
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