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. 2023 Jan 30;12:5. doi: 10.1186/s40035-023-00337-1

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© The Author(s) 2023, corrected publication 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Putative mechanisms of the link between COVID-19 and Parkinson's disease (PD). With the aid of TMPRSS2, the S protein of SARS-CoV-2 binds with ACE2 to enter the host cell. The SARS-CoV-2 virus may affect the midbrain in the following ways: vascular damage (BBB breakdown), systemic inflammation, and direct neuroinvasion, which then induce neuroinflammation, excessive oxidative stress, abnormal immune response, and aggregation of α-synuclein, leading to dopaminergic neuronal death and PD. ACE2: angiotensin-converting enzyme 2; α-syn: a-synuclein; BBB: blood–brain barrier; COVID-19: Coronavirus disease 2019; NRP1: neuropilin 1; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; TMPRSS2: transmembrane serine protease 2