| First Author | Fujita Y | Year | 2020 |
| Journal | Neuroscience | Volume | 443 |
| Pages | 1-7 | PubMed ID | 32682823 |
| Mgi Jnum | J:298365 | Mgi Id | MGI:6478605 |
| Doi | 10.1016/j.neuroscience.2020.07.016 | Citation | Fujita Y, et al. (2020) Engulfment of Toxic Amyloid beta-protein in Neurons and Astrocytes Mediated by MEGF10. Neuroscience 443:1-7 |
| abstractText | Amyloid-beta proteins (A beta), including Abeta42 and A beta 43, are known pathogenesis factors of Alzheimer's disease (AD). Unwanted substances in the brain, including A beta, are generally removed by microglia, astrocytes, or neurons via a phagocytosis receptor. We observed that neurons and astrocytes engulfed A beta 42 and A beta 43, which are more neurotoxic than A beta 40. We previously showed that multiple-EGF like domains 10 (MEGF10) plays an important role in apoptotic cell elimination and is expressed in mammalian neurons and astrocytes. Therefore, we assessed whether MEGF10 is involved in A beta42 and A beta43 engulfment in MEGF10-expressing neurons and astrocytes. We found that MEGF10-expressing astrocytes and neurons engulfed A beta42 and A beta43 but not A beta40. Furthermore, incubation of the neurons and astrocytes with A beta42 and A beta43a ugmented MEGF10 phosphorylation; however, incubation with A beta40 did not have this augmenting effect. Our findings suggest that MEGF10 plays a phagocytosis receptor function for A beta42 and A beta43 in neurons and astrocytes. |
