Mutant mice with small amounts of BubR1 display accelerated age-related gliosis

Tyler K. Hartman, Thomas M. Wengenack, Joseph F. Poduslo, Jan M. van Deursen

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


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 protein (BubR1H/H mice) develop several early aging-associated phenotypes. The phenotype within the brain of BubR1H/H mice has not yet been established. Here we show that BubR1H/H mice exhibit features of age-related cerebral degeneration. We found that glial fibrillary acidic protein (GFAP), a marker of reactive astrogliosis, was expressed at increased levels in the cortex and thalamus of BubR1H/H mice as early as 1 month of age. Furthermore, CD11b, a marker of microgliosis, was markedly elevated in the cortex and hippocampus of BubR1H/H mice at 5 months of age. Levels of both GFAP and CD11b further increased with age. Our results demonstrate that BubR1 acts to prevent cerebral gliosis of both astrocytes and microglial cells, and suggest a role for BubR1 in the aging process of the brain.

Original languageEnglish (US)
Pages (from-to)921-927
Number of pages7
JournalNeurobiology of aging
Issue number6
StatePublished - Jun 2007


  • Astrocyte
  • BubR1
  • CD11b
  • GFAP
  • Gliosis
  • Microglia

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology


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