• Yu Fujita, Tomoji Maeda, Chiharu Sato, Masaya Sato, Hatsune Hatakeyama, Yume Ota, Nozomi Iwabuchi, Komaki Tatesawa, Ayako Nomura, Kun Zou, and Hiroto Komano.
• Department of Neuroscience, School of Pharmacy, Iwate Medical University, 2-1-1 Idaidori, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan. Electronic address: yufujita@iwate-med.ac.jp.
• Neuroscience. 2020 Sep 1; 443: 1-7.

AbstractAmyloid-β proteins (A β), including Aβ42 and A β 43, are known pathogenesis factors of Alzheimer's disease (AD). Unwanted substances in the brain, including A β, are generally removed by microglia, astrocytes, or neurons via a phagocytosis receptor. We observed that neurons and astrocytes engulfed A β 42 and A β 43, which are more neurotoxic than A β 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 β42 and A β43 engulfment in MEGF10-expressing neurons and astrocytes. We found that MEGF10-expressing astrocytes and neurons engulfed A β42 and A β43 but not A β40. Furthermore, incubation of the neurons and astrocytes with A β42 and A β43a ugmented MEGF10 phosphorylation; however, incubation with A β40 did not have this augmenting effect. Our findings suggest that MEGF10 plays a phagocytosis receptor function for A β42 and A β43 in neurons and astrocytes.Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

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