Is COVID-19 a Perfect Storm for Parkinson's Disease?

Abstract

Three recent case reports (by Méndez-Guerrero et al.,Cohen et al., and Faber et al.) describe the development of acute parkinsonism following coronavirus disease 2019 (COVID-19). We discuss possible underlying cellular and molecular mechanisms, and whether COVID-19 might be associated with elevated long-term risk of Parkinson's disease (PD).

Keywords: SARS-CoV-2; alpha-synuclein; dopamine; neurodegeneration; neuroinflammation.

Figure 1

Schematic Illustration of How Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection Might Lead to Increased Parkinson’s Disease (PD) Risk. (A) Initial viral infection of the respiratory tract and/or the gut in patients with coronavirus disease 2019 (COVID-19) could affect the brain in three ways: through vascular damage; systemic inflammation; and direct neuroinvasion (e.g., via the olfactory system or vagal nerve), which each might act alone or in concert. Possible acute brain changes that can develop as a consequence, as well as longer term ones, are listed. Three recent case reports [3., 4., 5.] described the development of acute parkinsonism following COVID-19. These emerging findings suggest that SARS-CoV-2 infection leads to acute parkinsonism in certain cases, and raises the question of whether COVID-19 also elevates PD risk in the long term. Several of the brain changes that are commonly seen in PD (B) have also been observed following infection with SARS-CoV-2 or other related viruses, although fundamental questions remain regarding possible causal/mechanistic links. Figure created using Biorender (Biorender.com) with input from Gabriela Mercado and Sonia George.