1. Microglia: Senescence Impairs Clearance of Myelin Debris
Peter Thériault, Serge Rivest 
Current Biology 
Volume 26, Issue 16, Pages R772-R775 (August 2016)
DOI: /j.cub
Copyright © 2016 Elsevier Ltd Terms and Conditions

2. Figure 1
Myelin breakdown promotes microglia immune dysfunction and senescence.
Neurons are surrounded by myelin sheaths produced by oligodendrocytes. Myelin fragmentation occurs in normal aging (WT), Rab7 knockout, cuprizone-fed and Pelizaeus-Merzbacher disease (PMD) mice and leads to aggregation of myelin basic protein (MBP). Microglia are defined as ionized calcium binding adaptor molecule 1 (Iba1)-positive cells. Quiescent microglia are highly ramified and acquire an amoeboid shape once activated. Activated microglia upregulate surface markers involved in phagocytic activity, including macrophage antigen complex (Mac)-2 and CD68. Phagocytosis by activated microglia leads to aggregation of MBP, which in turn promotes the formation of lysosomal inclusions due to their impaired degradative capacities. These lipofuscin granules lead to microglial senescence and immune dysfunction as seen by an upregulation of class II major histocompatibility complex (MHC-II).
Current Biology  , R772-R775DOI: ( /j.cub )
Copyright © 2016 Elsevier Ltd Terms and Conditions