Ontology highlight
ABSTRACT: Background
Alzheimer's disease (AD) causes substantial medical and societal burden with no therapies ameliorating cognitive deficits. Centralized pathologies involving amyloids, neurofibrillary tangles, and neuroinflammatory pathways are being investigated to identify disease-modifying targets for AD. Cyclooxygenase-2 (COX-2) is one of the potential neuroinflammatory agents involved in AD progression. However, chronic use of COX-2 inhibitors in patients produced adverse cardiovascular effects. We asked whether inhibition of EP2 receptors, downstream of the COX-2 signaling pathway, can ameliorate neuroinflammation in AD brains in presence or absence of a secondary inflammatory stimuli.Methods
We treated 5xFAD mice and their non-transgenic (nTg) littermates in presence or abs
SUBMITTER: Banik A
PROVIDER: S-EPMC8605573 | biostudies-literature | 2021 Nov
REPOSITORIES: biostudies-literature