Impact of Glucocorticoids on Neuroinflammation in the TgF344‐AD Rat Model
Our initial results indicate that, despite no changes in glial marker levels, the treatment reduced C1qB levels while paradoxically increasing TNF-α in the TgF344-AD model. Since both TNF-α and C1qB are predominantly secreted by microglia, further studies are warranted to investigate whether dexamethasone induces a distinct microglial phenotype. Additional experiments are necessary to determine if these changes signify a shift in immune balance and whether they have protective or detrimental effects.
Authors
- Christian Limberger (ORCID: https://orcid.org/0000-0002-5160-3886)
- Rodrigo Sebben Paes (ORCID: https://orcid.org/0000-0002-2330-4862)
- Gabriel Bueno Martins (ORCID: https://orcid.org/0000-0003-3645-0276)
- Gabriela Mantovani Baldasso
- Roberta dos Santos de Oliveira
- Ramon Bertoldi de Souza
- Mariana Radaelli Schmaedek
- Eduardo R. Zimmer
- Gabriel Lermen Hoffmeister
Institutions
- Universidade Federal do Rio Grande do Sul (BR)
- Instituto do Cérebro (BR)
- Pontifícia Universidade Católica do Rio Grande do Sul (BR)
- McGill University (CA)
Publication Details
- Journal
- Alzheimer s & Dementia
- Published
- 2025-12-01
- DOI
- https://doi.org/10.1002/alz70855_103076
- Primary Topic
- Alzheimer's disease research and treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00