| First Author | Wu W | Year | 2025 |
| Journal | Nat Commun | Volume | 16 |
| Issue | 1 | Pages | 63 |
| PubMed ID | 39747869 | Mgi Jnum | J:361218 |
| Mgi Id | MGI:7851518 | Doi | 10.1038/s41467-024-55678-w |
| Citation | Wu W, et al. (2025) Modulation of glymphatic system by visual circuit activation alleviates memory impairment and apathy in a mouse model of Alzheimer's disease. Nat Commun 16(1):63 |
| abstractText | Alzheimer's disease is characterized by progressive amyloid deposition and cognitive decline, yet the pathological mechanisms and treatments remain elusive. Here we report the therapeutic potential of low-intensity 40 hertz blue light exposure in a 5xFAD mouse model of Alzheimer's disease. Our findings reveal that light treatment prevents memory decline in 4-month-old 5xFAD mice and motivation loss in 14-month-old 5xFAD mice, accompanied by restoration of glial water channel aquaporin-4 polarity, improved brain drainage efficiency, and a reduction in hippocampal lipid accumulation. We further demonstrate the beneficial effects of 40 hertz blue light are mediated through the activation of the vLGN/IGL-Re visual circuit. Notably, concomitant use of anti-Abeta antibody with 40 hertz blue light demonstrates improved soluble Abeta clearance and cognitive performance in 5xFAD mice. These findings offer functional evidence on the therapeutic effects of 40 hertz blue light in Abeta-related pathologies and suggest its potential as a supplementary strategy to augment the efficacy of antibody-based therapy. |
