# The Onset of Creutzfeldt–Jakob Disease After COVID-19: Navigating the Diagnostic Challenges and Clinical Evolution

**Authors:** Ahmet Z. Burakgazi

PMC · DOI: 10.1155/crnm/6617766 · 2025-10-23

## TL;DR

A woman developed Creutzfeldt–Jakob disease after recovering from COVID-19, highlighting the difficulty in diagnosing prion diseases among postviral neurological conditions.

## Contribution

This case emphasizes the diagnostic challenges of distinguishing CJD from post-COVID neurological complications.

## Key findings

- The patient showed rapid neurocognitive decline with MRI and EEG findings consistent with CJD.
- CSF analysis revealed elevated tau and 14-3-3 proteins and positive RT-QuIC, confirming CJD.
- Treatment with methylprednisolone and IVIG failed to halt disease progression.

## Abstract

This case report presents a 47-year-old female who developed Creutzfeldt–Jakob disease (CJD) in a patient who had recently experienced a COVID-19 infection. The patient initially experienced speech changes and cognitive decline approximately 4-5 weeks after recovering from COVID-19. Over the course of several months, her condition rapidly deteriorated, progressing to severe neurocognitive decline, including catatonia, aggression, and delusions. Diagnostic findings included cortical ribboning on MRI, generalized periodic discharges on EEG, and elevated tau and 14-3-3 proteins with positive RT-QuIC in CSF analysis. Despite various treatments, including methylprednisolone and IVIG, the patient's condition worsened, leading to hospice care within a year of symptom onset. This case illustrates the diagnostic challenges in distinguishing prion diseases from other postviral complications, particularly when presuming a parainfectious inflammatory process without supporting evidence, which may delay definitive testing such as RT-QuIC. No causal relationship between COVID-19 and CJD can be established from this single case. This report underlines the need for further research into potential post-COVID-19 neurological complications.

## Linked entities

- **Proteins:** MAPT (microtubule associated protein tau)
- **Diseases:** Creutzfeldt–Jakob disease (MONDO:0005357), COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, YWHAQ (tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein theta) [NCBI Gene 10971] {aka 14-3-3, 1C5, HS1}
- **Diseases:** catatonia (MESH:D002389), post-COVID-19 neurological complications (MESH:D000094024), inflammatory (MESH:D007249), cognitive decline (MESH:D003072), neurocognitive decline (MESH:D060825), CJD (MESH:D007562), COVID-19 (MESH:D000086382), aggression (MESH:D010554), delusions (MESH:D063726), prion diseases (MESH:D017096)
- **Chemicals:** methylprednisolone (MESH:D008775)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12575042/full.md

---
Source: https://tomesphere.com/paper/PMC12575042