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Human Neural Organoids for Studying Brain Cancer and Neurodegenerative Diseases
Published on: June 28, 2019
SARS-CoV-2 Infection Induces Dopaminergic Neuronal Loss in Midbrain Organoids
Javier Jarazo1,2, Eveline Santos da Silva3, Enrico Glaab4
1Developmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine University of Luxembourg, Esch-sur-Alzette, Luxembourg.
Journal of Neurochemistry
|May 25, 2026
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) selectively infects and damages dopaminergic neurons in human midbrain organoids. This study reveals persistent molecular changes, offering insights into COVID-19 neurological effects.
Area of Science:
- Neuroscience
- Virology
- Molecular Biology
Background:
- COVID-19 primarily causes respiratory illness, but SARS-CoV-2 neurological effects are increasingly reported.
- Dopaminergic neurons are crucial for motor control and are implicated in neurodegenerative diseases.
Purpose of the Study:
- To investigate the impact of SARS-CoV-2 on human midbrain organoids, focusing on dopaminergic neurons.
- To identify cellular and molecular changes induced by SARS-CoV-2 infection over time.
Main Methods:
- Human midbrain organoids were exposed to SARS-CoV-2.
- Immunofluorescence microscopy and RNA sequencing were used to analyze cellular and molecular changes at 4 and 28 days post-infection.
Main Results:
- SARS-CoV-2 preferentially infected tyrosine hydroxylase-positive (TH+) dopaminergic neurons, causing neurite fragmentation and cellular stress.
- Transcriptomic analysis revealed dysregulated pathways including cell stress, DNA damage, neurodevelopment, and neuronal survival.
- Persistent alterations in vesicle trafficking, Notch signaling, and mitochondrial function were observed at 28 days post-infection.
Conclusions:
- Dopaminergic neurons exhibit selective vulnerability to SARS-CoV-2 infection.
- Persistent molecular alterations suggest potential long-term neurological consequences of COVID-19.
- Findings provide mechanistic insights into SARS-CoV-2-induced neuroinflammation and neuronal dysfunction.
