| First Author | Rajani RM | Year | 2024 |
| Journal | PLoS Biol | Volume | 22 |
| Issue | 7 | Pages | e3002727 |
| PubMed ID | 39042667 | Mgi Jnum | J:361092 |
| Mgi Id | MGI:7704652 | Doi | 10.1371/journal.pbio.3002727 |
| Citation | Rajani RM, et al. (2024) Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer's disease. PLoS Biol 22(7):e3002727 |
| abstractText | Reduction of amyloid beta (Abeta) has been shown to be effective in treating Alzheimer's disease (AD), but the underlying assumption that neurons are the main source of pathogenic Abeta is untested. Here, we challenge this prevailing belief by demonstrating that oligodendrocytes are an important source of Abeta in the human brain and play a key role in promoting abnormal neuronal hyperactivity in an AD knock-in mouse model. We show that selectively suppressing oligodendrocyte Abeta production improves AD brain pathology and restores neuronal function in the mouse model in vivo. Our findings suggest that targeting oligodendrocyte Abeta production could be a promising therapeutic strategy for treating AD. |
