Pathogenesis of Post-COVID-19 Parkinsonism and Parkinson's D | 96608

मल्टीपल स्केलेरोसिस जर्नल

ISSN - 2376-0389


Pathogenesis of Post-COVID-19 Parkinsonism and Parkinson's Disease

Jin Yong

After Alzheimer's disease, Parkinson's disease (PD) is the most common neurological condition worldwide. The hallmarks of Parkinson's disease (PD) are misfolded alpha-synuclein aggregation and dopaminergic neuron degeneration in the substantia nigra pars compacta, along with both motor and non-motor symptoms. A post-infection parkinsonian phenotype's presence has been connected to several viruses. As a result of the emergence of the severe acute respiratory syndrome coronavirus-2 (SARSCoV-2) infection, the 2019 coronavirus disease (COVID-19), which initially manifested as novel pneumonia, has developed into a complex syndrome with a variety of clinical manifestations, including subtle and potentially long-lasting neurological sequelae. Exosomes are extracellular nanovesicles that play essential roles in intercellular communication in pathological situations. They carry a complex cargo of active biomolecules. Exosomes are a dependable method of misfolded protein transfer that aid in the pathophysiology and diagnosis of Parkinson's disease. Here, we review current research that suggests PD and SARS-CoV-2 infection share several clinical symptoms as well as inflammatory and molecular mechanisms. We continue to speculate that these commonalities may be represented in exosomal cargo that is altered by the virus in connection to the severity of the sickness. The SARS-CoV-2-related exosomal cargo moves from the brain to the periphery and carries SARS-CoV-2 RNA, viral proteins, inflammatory mediators, and modified host proteins that may act as promoters of neurodegenerative and neuroinflammatory cascades and eventually result in the development of parkinsonism and PD.