| First Author | Catchpole I | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 6 | Pages | e65518 |
| PubMed ID | 23799019 | Mgi Jnum | J:203471 |
| Mgi Id | MGI:5527060 | Doi | 10.1371/journal.pone.0065518 |
| Citation | Catchpole I, et al. (2013) Systemic administration of Abeta mAb reduces retinal deposition of Abeta and activated complement C3 in age-related macular degeneration mouse model. PLoS One 8(6):e65518 |
| abstractText | Age-related macular degeneration (AMD) is a leading cause of legal blindness in the Western world. There are effective treatments for the vascular complications of neo-vascular AMD, but no effective therapies are available for the dry/atrophic form of the disease. A previously described transgenic CFH-gene deficient mouse model, (cfh-/-), shows hallmarks of early AMD. The ocular phenotype has been further analysed to demonstrate amyloid beta (Abeta) rich basement membrane deposits associated with activated complement C3. Cfh-/- mice were treated systemically in both prophylactic and therapeutic regimes with an anti-Abeta monoclonal antibody (mAb), 6F6, to determine the effect on the cfh-/- retinal phenotype. Prophylactic treatment with 6F6 demonstrated a dose dependent reduction in the accumulation of both Abeta and activated C3 deposition. A similar reduction in the retinal endpoints could be seen after therapeutic treatment. Serum Abeta levels after systemic administration of 6F6 show accumulation of Abeta in the periphery suggestive of a peripheral sink mechanism. In summary, anti-Abeta mAb treatment can partially prevent or reverse ocular phenotypes of the cfh-/- mouse. The data support this therapeutic approach in humans potentially modulating two key elements in the pathogenesis of AMD - Abeta and activated, complement C3. |
