# Neuroimmune activation in temporal lobe epilepsy patients with worsening seizure following the COVID-19 pandemic: A [18F]DPA-714 PET/MR study

**Authors:** Ling Xiao, Li Qin, Tao Jiang, Ming Qu, Manliu Hou, Yongxiang Tang, Shuo Hu, Li Feng

PMC · DOI: 10.1126/sciadv.adu5874 · Science Advances · 2026-01-30

## TL;DR

This study shows that people with temporal lobe epilepsy who experience worse seizures after COVID-19 have increased brain inflammation and elevated blood inflammatory markers.

## Contribution

The study is the first to demonstrate widespread neuroinflammation and its correlation with blood inflammatory markers in post–COVID-19 active TLE using [18F]DPA-714 PET.

## Key findings

- Post–COVID-19 active TLE patients show widespread neuroinflammation in the brain.
- Plasma levels of IL-1β, IL-10, and IFN-γ correlate strongly with neuroimmune activation.
- Combining plasma inflammatory markers with TSPO PET could improve clinical diagnosis and monitoring of TLE.

## Abstract

Patients with temporal lobe epilepsy (TLE) frequently experience worsening epilepsy following COVID-19, referred to as post–COVID-19 active TLE. While neuroinflammatory changes are suspected in these patients, measurements of both central and systemic inflammation in the brain remain unexplored. We investigate whether the translocator protein standardized uptake value ratio (TSPO SUVr), a quantifiable marker of neuroinflammation using positron emission tomography (PET), is elevated in the brains of patients with post–COVID-19 active TLE. In addition, we examine correlations between TSPO SUVr and inflammatory factors to identify potential peripheral blood inflammatory predictors of post–COVID-19 active epilepsy. Our study highlights the presence of widespread neuroinflammation in the brain and increased levels of inflammatory cytokines in the plasma of individuals with post–COVID-19 active TLE. Furthermore, strong correlations between plasma levels of interleukin-1β (IL-1β), IL-10, and interferon-γ (IFN-γ) and neuroimmune activation suggest the potential for integrating plasma inflammatory factors with TSPO PET as a dependable approach for clinical diagnosis, dynamic monitoring, and assessment of immune-based therapeutic efficacy in TLE-associated neuroinflammation.

TSPO PET and inflammatory markers reveal spread neuroinflammation in temporal lobe epilepsy with seizure worsening after COVID-19.

## Linked entities

- **Proteins:** IL1B (interleukin 1 beta), IL10 (interleukin 10), IFNG (interferon gamma)
- **Diseases:** temporal lobe epilepsy (MONDO:0005115), COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** TSPO (translocator protein) [NCBI Gene 706] {aka BPBS, BZRP, DBI, IBP, MBR, PBR}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, GAD1 (glutamate decarboxylase 1) [NCBI Gene 2571] {aka CPSQ1, DEE89, GAD, GAD-67, SCP}, CASP1 (caspase 1) [NCBI Gene 834] {aka ICE, IL1BC, P45}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, AIF1 (allograft inflammatory factor 1) [NCBI Gene 199] {aka AIF-1, IBA1, IRT-1, IRT1}
- **Diseases:** structural abnormalities (MESH:C566527), inflammation (MESH:D007249), post-COVID-19 (MESH:D000094024), drug-resistant epilepsy (MESH:D000069279), anxiety (MESH:D001007), focal status epilepticus (MESH:D013226), vasoocclusive lesions (MESH:D009059), TLE (MESH:D004833), neuropsychiatric diseases (MESH:D004194), cognitive impairment (MESH:D003072), epileptic injury (MESH:D014947), depression (MESH:D003866), COVID-19 (MESH:D000086382), Alzheimer's disease (MESH:D000544), cytokine storm (MESH:D000080424), inflammatory syndrome (MESH:D018746), epilepsy (MESH:D004827), cytotoxic (MESH:D064420), drug addiction (MESH:D019966), neuronal injury (MESH:D009410), tumor (MESH:D009369), Seizures (MESH:D012640), hypoxic (MESH:D002534), multisystem (MESH:D019578), neurological or psychiatric disorders (MESH:D001523), Neuroinflammation (MESH:D000090862), infected (MESH:D007239), autoimmune encephalitis (MESH:D020274), traumatic brain injury (MESH:D000070642), depressive and/or cognitive symptoms (MESH:D019954), autoimmune epilepsy (MESH:D001327)
- **Chemicals:** adenosine triphosphate (MESH:D000255), reactive oxygen species (MESH:D017382), pilocarpine (MESH:D010862), midazolam (MESH:D008874), 3DT1 (-), glutamate (MESH:D018698), methylprednisolone (MESH:D008775)
- **Species:** Homo sapiens (human, species) [taxon 9606], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Mutations:** rs6971

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12857733/full.md

## References

70 references — full list in the complete paper: https://tomesphere.com/paper/PMC12857733/full.md

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Source: https://tomesphere.com/paper/PMC12857733