TREM2 supports neuronal protection and microglial reactivity without an effect on misfolded protein deposition in chronic neurodegenerative prion disease
We conclude that during brain infection with prions, TREM2 supports microglial reactive changes associated with resilience to neuronal loss independently of affecting misfolded PrP deposition. These data imply that TREM2 status may be an important influence on the downstream response to CNS proteinopathy, which alters the susceptibility of neurons and brain tissue to proteinopathy-induced degenerative changes.
Authors
- Jimena Monzón‐Sandoval (ORCID: https://orcid.org/0000-0002-4190-2188)
- Jean Manson (ORCID: https://orcid.org/0000-0002-0175-9890)
- Barry Bradford (ORCID: https://orcid.org/0000-0002-4007-1685)
- Pedro Piccardo
- Alessio Alfieri (ORCID: https://orcid.org/0000-0002-4572-3208)
- Aileen Boyle
- Barry W. McColl (ORCID: https://orcid.org/0000-0002-0521-9656)
- Neil A. Mabbott (ORCID: https://orcid.org/0000-0001-7395-1796)
- Sarah M. Carpanini (ORCID: https://orcid.org/0000-0002-7609-7529)
- Aleksandra Pokrovskaya
- Deborah A. Brown
Institutions
- Roslin Institute (GB)
- UK Dementia Research Institute (GB)
- Cardiff University (GB)
- University of Edinburgh (GB)
Publication Details
- Journal
- Frontiers in Neuroscience
- Published
- 2025-05-07
- DOI
- https://doi.org/10.3389/fnins.2025.1525017
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00