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Mouse microglia show in vitro increased ingestion of Aβ after activation of TLR2, TLR4 or TLR9.
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In mice lacking CD200, microglia show evidence of being morphologically activated, and these mice are prone to a more rapid onset of clinical symptoms in EAE (experimental allergic encephalomyelitis) (Hoek et al., 2000).
In addition, compared with retinal microglia in young mice, aged microglia showed significantly smaller and fewer branched processes, slower process formation and motility, and a poor response to laser-induced focal tissue injury (Damani et al., 2011).
Interestingly, G4 mTerc−/− microglia show an increase in p21 mRNA.
While only a small population of microglia showed soma movement in adult mice, the microglia population with soma movement was increased in aged mice.
At 7 days after OVA injection, a large number of macrophages and microglia showed increased expression of FcγRII/III, while non-immunized control mice showed minimal expression of FcγRs.
Microglia showed ameboid shapes and increased in number in the spinal cord of SOD1G93A mice.
CNS microglia showed substantial inflammatory activity.
Notably, 10‐month‐old G3 mTerc−/− microglia showed an enhanced pro‐inflammatory response higher than 24‐month‐old wild‐type microglia.
Iron-containing microglia showed signs of cell degeneration.
However, after intraperitoneal injection of bacterial lipopolysaccharide (LPS), G3 mTerc−/− microglia mice show an enhanced pro‐inflammatory response.
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