Blood-derived plasminogen drives brain inflammation and plaque deposition in a mouse model of Alzheimer's disease.
Ontology highlight
ABSTRACT: Two of the most predominant features of the Alzheimer's disease (AD) brain are deposition of β-amyloid (Aβ) plaques and inflammation. The mechanism behind these pathologies remains unknown, but there is evidence to suggest that inflammation may predate the deposition of Aβ. Furthermore, immune activation is increasingly being recognized as a major contributor to the pathogenesis of the disease, and disorders involving systemic inflammation, such as infection, aging, obesity, atherosclerosis, diabetes, and depression are risk factors for the development of AD. Plasminogen (PLG) is primarily a blood protein synthesized in the liver, which when cleaved into its active form, plasmin (PL), plays roles in fibrinolysis, wound healing, cell signaling, and inflammatory regulation. Here we show that
SUBMITTER: Baker SK
PROVIDER: S-EPMC6187132 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature
ACCESS DATA