Mutant mice with small amounts of BubR1 display accelerated age-related gliosis.
作者： Tyler K. Hartman , Thomas M. Wengenack , Joseph F. Poduslo , Jan M. van Deursen
DOI: 10.1016/J.NEUROBIOLAGING.2006.05.012
关键词:
摘要: Abstract Aging is an intricate biological process thought to involve multiple molecular pathways. The spindle assembly checkpoint protein BubR1 has recently been implicated in aging since mutant mice that have small amounts of this (BubR1H/H mice) develop several early aging-associated phenotypes. phenotype within the brain BubR1H/H not yet established. Here we show exhibit features age-related cerebral degeneration. We found glial fibrillary acidic (GFAP), a marker reactive astrogliosis, was expressed at increased levels cortex and thalamus as 1 month age. Furthermore, CD11b, microgliosis, markedly elevated hippocampus 5 months Levels both GFAP CD11b further with Our results demonstrate acts prevent gliosis astrocytes microglial cells, suggest role for brain.
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