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PP2A subunit PPP2R2C is downregulated in the brains of Alzheimer's transgenic mice

Waiian Leong1,2, Wei Xu1, Bo Wang1,2

  • 1Shanghai Ruijin Hospital, Shanghai Ruijin Hospital North, Affiliated to Shanghai Jiaotong University School of Medicine, International Laboratory in Hematology, Aging and Cancer, State Key Laboratory of Medical Genomics, Pôle Sino-Français de Recherche en Sciences du Vivant et Génomique, Shanghai, P.R. China.

Aging
|April 16, 2020
PubMed

Insights

Dysregulation of the PPP2R2C gene, a key player in brain phosphatase activity, is linked to Alzheimer's disease (AD). Lowering PPP2R2C expression in aged AD mouse brains suggests it may be a therapeutic target for dementia.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Protein phosphatase 2A (PP2A) is implicated in tau-related cognitive decline in Alzheimer's disease (AD).
  • Understanding PP2A subunit dysregulation in AD is crucial for developing targeted therapies.
  • While PR55/Bα is a known tau phosphatase, the role of other brain-specific PP2A subunits in tau dephosphorylation is unclear.

Purpose of the Study:

  • To investigate the role of the brain-specific PP2A regulatory subunit PR55/Bγ (encoded by the PPP2R2C gene) in Alzheimer's disease.
  • To determine the spatiotemporal expression patterns of PPP2R2C in wild-type (Wt) and transgenic AD mouse models.
  • To assess the impact of PPP2R2C expression on PP2A activity and tau dephosphorylation.

Main Methods:

  • Differential spatiotemporal expression analysis of PPP2R2C in aged Wt and transgenic AD mouse brains.
  • In vitro studies using cultured cells to examine the effect of PPP2R2C expression on PP2A activity and tau dephosphorylation.

Main Results:

  • PPP2R2C expression was found to be downregulated in the aged AD mouse brain compared to the Wt mouse brain.
  • Experimental manipulation of PPP2R2C expression in cultured cells demonstrated its regulatory role in PP2A activity.
  • PPP2R2C expression was shown to influence the level of tau dephosphorylation in cellular models.

Conclusions:

  • Dysregulation of PPP2R2C expression may contribute to the pathogenesis of Alzheimer's disease.
  • Targeting PPP2R2C expression or activity presents a potential therapeutic strategy for AD and other tauopathies.
  • Further research into PPP2R2C's role could lead to novel treatments for brain dementia disorders.
Keywords:
Alzheimer’s diseasePP2A phosphatasePPP2R2Ctau phosphorylation

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