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SARS-CoV-2 infection exacerbates the cellular pathology of Parkinsons disease in human dopaminergic neurons and a mouse model.
- Lee, Bina;
- Choi, Ha;
- Che, Young;
- Ko, Myungjun;
- Seong, Hye;
- Jo, Min;
- Kim, Seon-Hee;
- Song, Chieun;
- Yoon, Subeen;
- Choi, Jiwoo;
- Kim, Jeong;
- Kim, Minkyeong;
- Lee, Min;
- Park, Sang;
- Kim, Hye;
- Kim, Seong;
- Moon, Do;
- Lee, Sun;
- Park, Jae-Hoon;
- Yeo, Seung-Geun;
- Everson, Richard;
- Kim, Young;
- Hong, Kyung-Wook;
- Roh, In-Soon;
- Lyoo, Kwang-Soo;
- Kim, Yong;
- Yun, Seung
- et al.
Published Web Location
https://doi.org/10.1016/j.xcrm.2024.101570Abstract
While an association between Parkinsons disease (PD) and viral infections has been recognized, the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on PD progression remains unclear. Here, we demonstrate that SARS-CoV-2 infection heightens the risk of PD using human embryonic stem cell (hESC)-derived dopaminergic (DA) neurons and a human angiotensin-converting enzyme 2 (hACE2) transgenic (Tg) mouse model. Our findings reveal that SARS-CoV-2 infection exacerbates PD susceptibility and cellular toxicity in DA neurons pre-treated with human preformed fibrils (hPFFs). Additionally, nasally delivered SARS-CoV-2 infects DA neurons in hACE2 Tg mice, aggravating the damage initiated by hPFFs. Mice infected with SARS-CoV-2 display persisting neuroinflammation even after the virus is no longer detectable in the brain. A comprehensive analysis suggests that the inflammatory response mediated by astrocytes and microglia could contribute to increased PD susceptibility associated with SARS-CoV-2. These findings advance our understanding of the potential long-term effects of SARS-CoV-2 infection on the progression of PD.
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