Age-related deregulation of TDP-43 after stroke enhances NF-κB-mediated inflammation and neuronal damage.

ABSTRACT:

Background

TDP-43 has been identified as a disease-associated protein in several chronic neurodegenerative disorders and increasing evidence suggests its potentially pathogenic role following brain injuries. Normally expressed in nucleus, under pathological conditions TDP-43 forms cytoplasmic ubiquitinated inclusions in which it is abnormally phosphorylated and cleaved to generate a 35 and a 25 kDa C-terminal fragments. In the present study, we investigated age-related expression patterns of TDP-43 in neurons and glia and its role as modulator of inflammation following ischemic injury.

Methods

Wild-type and TDP-43 transgenic mice of different age groups were subjected to transient middle cerebral artery occlusion. The role of TDP-43 in modulation of inflammation was assessed

SUBMITTER: Thammisetty SS 

PROVIDER: S-EPMC6230239 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature