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Brain Fog

Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19

Fekete R, Simats A, Bíró E, et al. Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19. Nat Neurosci. 2025;28(3):558-576. doi:10.1038/s41593-025-01871-z.

Impaired microglia function and vascular inflammation in COVID

  • Observational study evaluating Long COVID patients treated with H1/H2 antihistamines.

  • Reports improvement in fatigue, cognitive symptoms, tachycardia, and other systemic complaints.

  • Supports the hypothesis that mast cell activation contributes to Long COVID symptom persistence.

  • Suggests immune dysregulation—rather than viral persistence—may drive ongoing symptoms in a subset of patients.

Antihistamines improve cardiovascular manifestations and other symptoms of long-COVID attributed to mast cell activation

Salvucci F, Codella R, Coppola A, et al. Antihistamines improve cardiovascular manifestations and other symptoms of long-COVID attributed to mast cell activation. Front Cardiovasc Med. 2023;10:1202696. doi:10.3389/fcvm.2023.1202696.

Mast cell activation in Long COVID (related work)

  • Observational study evaluating Long COVID patients treated with H1/H2 antihistamines.

  • Reports improvement in fatigue, cognitive symptoms, tachycardia, and other systemic complaints.

  • Supports the hypothesis that mast cell activation contributes to Long COVID symptom persistence.

  • Suggests immune dysregulation—rather than viral persistence—may drive ongoing symptoms in a subset of patients.

Long Covid brain fog: a neuroinflammation phenomenon?

Kavanagh E. Long Covid brain fog: a neuroinflammation phenomenon? J Neuroinflammation. 2022;19(1):265. doi:10.1186/s12974-022-02665-6.

Neuroinflammation and Long COVID “brain fog”

  • Reviews evidence that persistent cognitive symptoms after COVID are linked to neuroinflammation rather than ongoing viral infection.

  • Highlights roles for microglial activation, cytokine signaling, and disrupted neuroimmune regulation.

  • Proposes that immune-mediated effects on synaptic function and neuronal metabolism can explain attention, memory, and processing-speed deficits.

  • Frames brain fog as a biological inflammatory process, not a psychological or functional complaint.