Background <p>It has been six years since the COVID-19 pandemic and, despite substantial advances in management, the disease sequelae known as long COVID continues to represent a significant medical and societal burden. Long COVID is characterised by persistent neurological and neurocognitive symptoms, including brain fog, memory deficits, attention impairments, and fatigue, lasting for months after acute SARS-CoV-2 infection.</p> Main body <p>In this review, we collated emerging neurological findings related to long COVID, discussing neurodegenerative processes associated with long COVID, potential clinical implications and research limitations. Neurological and neurocognitive manifestations arise through multiple mechanisms, including direct SARS-CoV-2 invasion of the central nervous system and peripheral lymphocyte infiltration. Additionally, neurovascular damage potentially contributes to neurodegeneration through neuronal injury, impaired neurogenesis, microvascular abnormality and sustained neuroinflammation.</p> Conclusion <p>Understanding the mechanisms underlying neurological and neurocognitive symptoms is essential for developing long-term monitoring strategies and targeted interventions to mitigate neurocognitive decline in individuals with long COVID.</p>

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Neurological impairment in long COVID: implications for neurodegenerative disease

  • Etianne Martini Sasso,
  • Natalie Eaton-Fitch,
  • Kiran Thapaliya,
  • Sonya Marshall-Gradisnik

摘要

Background

It has been six years since the COVID-19 pandemic and, despite substantial advances in management, the disease sequelae known as long COVID continues to represent a significant medical and societal burden. Long COVID is characterised by persistent neurological and neurocognitive symptoms, including brain fog, memory deficits, attention impairments, and fatigue, lasting for months after acute SARS-CoV-2 infection.

Main body

In this review, we collated emerging neurological findings related to long COVID, discussing neurodegenerative processes associated with long COVID, potential clinical implications and research limitations. Neurological and neurocognitive manifestations arise through multiple mechanisms, including direct SARS-CoV-2 invasion of the central nervous system and peripheral lymphocyte infiltration. Additionally, neurovascular damage potentially contributes to neurodegeneration through neuronal injury, impaired neurogenesis, microvascular abnormality and sustained neuroinflammation.

Conclusion

Understanding the mechanisms underlying neurological and neurocognitive symptoms is essential for developing long-term monitoring strategies and targeted interventions to mitigate neurocognitive decline in individuals with long COVID.