Can the 2019 Novel Coronavirus Cause Parkinson's Disease?

Abstract

The coronavirus disease 2019 (COVID-19) is a highly pathogenic viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2). SARS-Cov-2 has neuroinvasive capacities, given that it can spread from the respiratory tract to the nervous system. Certain viruses invade the central nervous system and release inflammatory cytokines, which can play a part in the development of the pathogenesis of Parkinson's disease (PD). This article proposes a hypothesis that viruses with viremia potential can cause PD. A recent study claims that SARS-Cov-2 shares similarities with severe acute respiratory syndrome coronavirus (SARS-Cov). This could be the reason why SARS-Cov and SARS-Cov-2 might occupy the same place in human brains.1 The nascent coronavirus uses mainly the same angiotensin-converting enzyme 2 (ACE2) receptor as the SARS-Cov. Activation of ACE-2 generates the angiotensin (1-7) that binds to the Mas receptor (Mas-R), providing anti-inflammatory and -fibrotic action. The ability of SARS-Cov-2 to penetrate and infect the human nervous system is based on the high expression of the ACE2 target throughout the brain.2 By binding on ACE2 receptor, the COVID-19 virus would decrease the effect of ACE2, thus aggravating inflammatory lesions (Fig. 1).3, 4 The movement to the brain by the 2019 novel coronavirus through the cribriform plate near the olfactory bulb may be an additional pathway for the virus to reach and infect the brain.5 Several acute neurological syndromes have been associated with coronaviruses. Recently, some researchers have confirmed the presence of SARS-Cov-2 in the cerebrospinal fluid of patients with COVID-19.4 Systemic inflammation triggered by SARS-Cov-2 infection may further contribute to neuroinflammatory processes and increase susceptibility to neurological syndromes, including severe encephalitis, and might produce chronic intermittent damage to the dopamine-producing neurons of the SN in humans.3 PD is characterized by alpha-synucleinopathy that affects all levels of the brain-gut axis, including the central, autonomic, and enteric nervous systems. Aggregation of the resulting alpha-synuclein (α-Syn) in the brain activates microglia, which causes an increase in oxidative stress that exacerbates neuroinflammation.6 Therefore, a contribution of viral infection, and, by implication, of viral-mediated neuroinflammation and α-synucleinopathy, is prominent and warrants a more thorough investigation of the probable impact of the 2019 novel coronavirus on PD progression. A potential role of the coronaviruses in the pathogenesis of postencephalic parkinsonism and PD is a future focus of study, including the mechanism by which the coronavirus selectively and persistently attacks a clinically important region of the brain. However, confounding variables, including the roles of both genetics and environmental exposures, must be considered in further research. The neurological examination of viral involvement must therefore be considered in health promotion and treatment strategies for SARS-Cov-2 victims. It will be pertinent to establish neurological and meticulous monitoring of patients who are confirmed as COVID-19 positive, using different diagnostic methods (α-Syn dosage, the imaging technique). Manuscript Preparation: A. Writing of the First Draft, B. Review and Critique. A.A.: A, B H.S.: A A.N.: A M.B.: A A.K.: A Y.B.: A, B M.N.: B Nothing to report.

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