Pharmacologic inhibition of reactive gliosis blocks TNF-α-mediated neuronal apoptosis.

ABSTRACT: Reactive gliosis is an early pathological feature common to most neurodegenerative diseases, yet its regulation and impact remain poorly understood. Normally astrocytes maintain a critical homeostatic balance. After stress or injury they undergo rapid parainflammatory activation, characterized by hypertrophy, and increased polymerization of type III intermediate filaments (IFs), particularly glial fibrillary acidic protein and vimentin. However, the consequences of IF dynamics in the adult CNS remains unclear, and no pharmacologic tools have been available to target this mechanism in vivo. The mammalian retina is an accessible model to study the regulation of astrocyte stress responses, and their influence on retinal neuronal homeostasis. In particular, our work and others have implicated

SUBMITTER: Livne-Bar I 

PROVIDER: S-EPMC5059876 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature