| First Author | Cao Q | Year | 2024 |
| Journal | J Exp Med | Volume | 221 |
| Issue | 11 | PubMed ID | 39316084 |
| Mgi Jnum | J:359168 | Mgi Id | MGI:7736137 |
| Doi | 10.1084/jem.20240386 | Citation | Cao Q, et al. (2024) Transport of beta-amyloid from brain to eye causes retinal degeneration in Alzheimer's disease. J Exp Med 221(11) |
| abstractText | The eye is closely connected to the brain, providing a unique window to detect pathological changes in the brain. In this study, we discovered beta-amyloid (Abeta) deposits along the ocular glymphatic system in patients with Alzheimer's disease (AD) and 5xFAD transgenic mouse model. Interestingly, Abeta from the brain can flow into the eyes along the optic nerve through cerebrospinal fluid (CSF), causing retinal degeneration. Abeta is mainly observed in the optic nerve sheath, the neural axon, and the perivascular space, which might represent the critical steps of the Abeta transportation from the brain to the eyes. Aquaporin-4 facilitates the influx of Abeta in brain-eye transport and out-excretion of the retina, and its absence or loss of polarity exacerbates brain-derived Abeta induced damage and visual impairment. These results revealed brain-to-eye Abeta transport as a major contributor to AD retinopathy, highlighting a new therapeutic avenue in ocular and neurodegenerative disease. |
