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SARS-CoV-2 infection exacerbates MTHFR deficiency, causing blood-brain barrier issues and neuroinflammation. This may increase Parkinson

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Area of Science:

  • Neuroscience
  • Virology
  • Genetics

Background:

  • Methylene tetrahydrofolate reductase (MTHFR) is vital for one-carbon metabolism, impacting neurotransmitter synthesis and DNA methylation.
  • MTHFR polymorphisms are linked to vascular dementia, Parkinson's disease (PD), and increased COVID-19 severity.
  • Mthfr-deficient mice exhibit cognitive deficits and increased PD-like pathology.

Purpose of the Study:

  • To investigate if SARS-CoV-2 infection accelerates vascular dementia and PD in MTHFR-deficient mice.
  • To model the impact of MTHFR deficiency on SARS-CoV-2-induced neurological effects.

Main Methods:

  • Mice with MTHFR deficiency (Mthfr+/-) and wild-type (WT) littermates were infected with mouse-adapted SARS-CoV-2 (MA10) or mock.
  • Mice were monitored for weight loss, and tissues were analyzed for viral load, inflammation, blood-brain barrier (BBB) integrity, and PD markers.
  • Plasma metabolomics was performed to assess biochemical changes.

Main Results:

  • MA10 infection caused comparable weight loss and lung viral titers in both Mthfr+/- and WT mice, with no detectable brain virus.
  • Mthfr+/- mice showed increased BBB disruption, neuroinflammation (IL-1β, microglia), and reduced plasma dopamine.
  • SARS-CoV-2 infection decreased dopaminergic neurons and tyrosine hydroxylase levels while increasing alpha-synuclein in Mthfr+/- mice.

Conclusions:

  • SARS-CoV-2 infection induces BBB dysfunction, neuroinflammation, and dopamine reduction in MTHFR-deficient mice.
  • The study suggests a heightened risk of Parkinson's disease progression in individuals with MTHFR deficiency following SARS-CoV-2 infection.