TREM2 supports neuronal protection and microglial reactivity without an effect on misfolded protein deposition in chronic neurodegenerative prion disease.

ABSTRACT:

Introduction

Triggering receptor expressed on myeloid cells-2 (TREM2) variants have been identified as risk factors for neurodegenerative disease, including Alzheimer's disease. TREM2 is a cell surface receptor on microglia that regulates homeostatic and immunomodulatory functions, including phagocytosis of apoptotic debris and the resolution of damage-associated inflammation. It remains unclear how TREM2 may mediate an influence on neurodegenerative disease, particularly in relation to key neuropathological hallmarks such as neuronal loss and proteinopathy.

Methods

We used the ME7 prion disease model to assess the role of TREM2 in the progression and pathology of neurodegenerative disease. Prion diseases are characterised by the accumulation of misfolded prion protei

SUBMITTER: Carpanini SM 

PROVIDER: S-EPMC12093410 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature