| First Author | Ioannou M | Year | 2023 |
| Journal | Biochem Biophys Res Commun | Volume | 675 |
| Pages | 78-84 | PubMed ID | 37454400 |
| Mgi Jnum | J:338546 | Mgi Id | MGI:7513571 |
| Doi | 10.1016/j.bbrc.2023.07.001 | Citation | Ioannou M, et al. (2023) Treatment of the CRND8 mouse model for cerebral amyloid angiopathy, exhibited increased levels of neuron specific enolase in brain tissue following long-term treatment with a modified C5a receptor agonist, accompanied by improved cognitive function. Biochem Biophys Res Commun 675:78-84 |
| abstractText | Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by amyloid plaques, neurofibrillary tangles, and cerebral amyloid angiopathy (CAA). CAA is a condition manifesting as amyloid deposits in the cerebral vasculature, eventually leading to microhemorrhage. Here, we have treated the CRND8 mouse model with the C5a agonist (EP67) in order to observe the effects on cerebral amyloidosis, CAA, and hyperphosphorylated tau. EP67 attaches to the C5a receptor on phagocytes and stimulates the engulfment and digestion of fibrillar and prefibrillar amyloid while exhibiting minimal inflammation. Older CRND8 mice and their respective controls were treated with EP67 for a prolonged period of time. Following treatment, the CRND8 mice displayed improved spatial memory, while both amyloid deposition and tau hyperphosphorylation were found to be diminished. |
