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GRK5 deficiency exaggerates inflammatory changes in TgAPPsw mice.

Longxuan Li1, Jun Liu, William Z Suo

  • 1Lab, for Alzheimer's Disease & Aging Res,, VA Med, Center, Kansas City, MO 64128, USA. longxuanlee2006@yahoo.com

Journal of Neuroinflammation
|June 5, 2008
PubMed
Summary

G-protein coupled receptor kinase-5 (GRK5) deficiency exacerbates microgliosis and astrogliosis in Alzheimer's disease models. This suggests GRK5 plays a protective role against neuroinflammation in the presence of amyloid-beta.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • G-protein coupled receptor kinase-5 (GRK5) deficiency is linked to early Alzheimer's disease (AD) pathogenesis.
  • GRK5 deficiency may augment microglial activation by sensitizing G-protein coupled receptors (GPCRs).
  • Previous studies showed GRK5 deficient mice lacked microgliosis, possibly due to absent inflammatory processes.

Purpose of the Study:

  • To investigate if GRK5 deficiency exaggerates microgliosis in TgAPPsw (Tg2576) mice.
  • To assess the role of GRK5 in neuroinflammation associated with fibrillar beta-amyloid (Abeta) and activated GPCR signaling.

Main Methods:

  • Utilized quantitative and qualitative immunochemistry.
  • Evaluated microgliosis and astrogliosis in GRK5 deficient TgAPPsw mice.

Main Results:

  • Inactivation of one GRK5 gene copy doubled microgliosis extent in TgAPPsw mice.
  • Significantly exaggerated astrogliosis was observed in hippocampus and cortex.
  • Activated microglia were found near fibrillar Abeta deposits.

Conclusions:

  • GRK5 deficiency significantly exacerbates microgliosis and astrogliosis in vivo.
  • This occurs in the presence of inflammatory initiators like excess fibrillar Abeta.
  • The findings highlight GRK5's role in modulating neuroinflammation in AD pathogenesis.