Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 10, 2026 52 minutes ago
A new murine study has found that SARS-CoV-2 infection can intensify abnormalities involving dopamine, brain immune cells and nerve-cell degeneration in a mouse model of early Parkinson’s disease. The effects were particularly pronounced in male mice, while females showed considerably greater resistance to neurological damage.
Murine research shows SARS-CoV-2 can amplify dopamine disruption, glial responses and Parkinson’s-related
brain damage, particularly in males
The findings provide new clues about how viral infection and existing Parkinson’s-related vulnerability could interact inside the brain.
Researchers Model Two Hits to the Brain
Researchers used K18-hACE2 mice, which carry the human ACE2 receptor that permits infection with SARS-CoV-2. Some animals first received MPTP, a neurotoxin widely used to create Parkinson’s-like damage because it targets the dopamine system.
Eleven days later, the mice were exposed to SARS-CoV-2. Scientists subsequently measured dopamine and its breakdown products and examined dopamine-producing neurons, nerve terminals, astrocytes and microglia.
The researchers were from the School of Medical Sciences, Faculty of Health, University of Victoria; Axe Neurosciences, Centre de recherche du CHU de Québec, Université Laval; Infectious Disease Research Center, Centre de recherche du CHU de Québec, Université Laval; Institute on Aging and Lifelong Health, University of Victoria; Centre for Advanced Materials and Related Technology, University of Victoria; and Department of Biochemistry and Molecular Biology, University of British Columbia, Canada.
COVID-19 Disrupted Dopamine Metabolism
One important discovery involved dopamine, a brain chemical essential for controlling movement and other functions. Parkinson’s develops as dopamine-producing neurons progressively deteriorate.
SARS-CoV-2 produced progressive disruption of dopamine metabolism in male mice by day 21. MPTP itself reduced dopamine, but males were more vulnerable than females. When SARS-CoV-2 was added to the MPTP-related damage, abnormalities involving dopamine metabolites became more pronounced in males.
As explained in this
Thailand Medical News report, the researchers concluded that the damage appeared largely additive rather than synergistic. This means SARS-CoV-2 appeared to add another damaging burden to an already vulnerable dopamine system rather than producing an unexpectedly multiplied effect.
Glial Cells Revealed Major Sex Differences
Researchers also discovered striking differences involving microglia and astrocytes. These glial cells help maintain the brain and participate in immune and inflammatory responses.
Male mice exposed to both MPTP and SARS-CoV-2 showed significant degeneration within the nigrostriatal pathway, the dopamine-producing brain system heavily affected by Parkinson’s. They also developed
strong astrocyte and microglial responses.
Microscopic examination revealed stressed and degenerating dopamine neurons in males. These cells showed shrinkage, abundant mitochondria and prominent Golgi structures, indicating substantial cellular stress. The abnormalities were especially noticeable following combined exposure.
Female mice, however, experienced comparatively little dopamine-related degeneration. Their microglia responded differently, becoming more clustered and showing an increased presence of amoeboid-like cells with enlarged cell bodies and retracted processes. Researchers believe these differing glial responses could help explain the contrasting vulnerability between sexes.
Important Limitations Remain
The researchers caution that this was an animal study using a specialized mouse model and MPTP rather than naturally developing Parkinson’s disease. The experiment was also relatively short. Future studies using longer observation periods and alpha-synuclein-based Parkinson’s models are needed, particularly because human and mouse glial responses can differ.
Conclusion
The findings suggest that SARS-CoV-2 infection can produce lasting changes in dopamine metabolism and glial activity and potentially add to existing Parkinson’s-related neurological damage, particularly in male mice. However, the study does not demonstrate that COVID-19 causes Parkinson’s disease in humans. Longer animal studies and carefully designed human investigations are essential to determine whether similar sex-specific brain changes occur after COVID-19 and whether they influence Parkinson’s development or progression.
The study findings were published in the peer reviewed journal: Movement Disorders.
https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.70454
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