| First Author | Cho MH | Year | 2014 |
| Journal | Autophagy | Volume | 10 |
| Issue | 10 | Pages | 1761-75 |
| PubMed ID | 25126727 | Mgi Jnum | J:303034 |
| Mgi Id | MGI:6511588 | Doi | 10.4161/auto.29647 |
| Citation | Cho MH, et al. (2014) Autophagy in microglia degrades extracellular beta-amyloid fibrils and regulates the NLRP3 inflammasome. Autophagy 10(10):1761-75 |
| abstractText | Accumulation of beta-amyloid (Abeta) and resultant inflammation are critical pathological features of Alzheimer disease (AD). Microglia, a primary immune cell in brain, ingests and degrades extracellular Abeta fibrils via the lysosomal system. Autophagy is a catabolic process that degrades native cellular components, however, the role of autophagy in Abeta degradation by microglia and its effects on AD are unknown. Here we demonstrate a novel role for autophagy in the clearance of extracellular Abeta fibrils by microglia and in the regulation of the Abeta-induced NLRP3 (NLR family, pyrin domain containing 3) inflammasome using microglia specific atg7 knockout mice and cell cultures. We found in microglial cultures that Abeta interacts with MAP1LC3B-II via OPTN/optineurin and is degraded by an autophagic process mediated by the PRKAA1 pathway. We anticipate that enhancing microglial autophagy may be a promising new therapeutic strategy for AD. |
