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Ptprd deficiency promotes tau hyperphosphorylation and impairs cognitive function in aged mice.

Analía Foncea1, Nayhara Franchini1, Isidora Tobar1

  • 1Centro de Biología Integrativa, Facultad de Ciencias, Universidad Mayor, Santiago, Chile.

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|May 6, 2025
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Summary

Loss of protein tyrosine phosphatase receptor delta (PTPRD) increases tau phosphorylation and cognitive decline in aging mice. PTPRD deficiency also promotes neuroinflammation and synaptic dysfunction, highlighting its protective role in tauopathies.

Keywords:
ABL1Cognitive impairmentMicrogliosisPTPRDSynaptic dysfunctionTau phosphorylationTauopathy

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Aberrant tau phosphorylation is central to neurodegenerative tauopathies, causing cognitive decline.
  • Protein tyrosine phosphatase receptor delta (PTPRD) is genetically linked to human tau pathology, but its precise role is unknown.
  • Understanding PTPRD's function is crucial for regulating tau phosphorylation and mitigating neurodegeneration.

Purpose of the Study:

  • To investigate the effects of PTPRD deficiency on tau phosphorylation.
  • To assess the impact of PTPRD loss on cognitive function, neuroinflammation, and synaptic integrity in aging mice.

Main Methods:

  • Utilized PTPRD knockout aging mouse models.
  • Analyzed tau phosphorylation levels and Abl1 kinase activity.
  • Conducted behavioral tests for learning and memory assessment.
  • Examined markers of microgliosis and synaptic proteins (e.g., PSD95).

Main Results:

  • PTPRD deficiency led to increased tau phosphorylation and Abl1 kinase activation, particularly in the hippocampus.
  • Mice lacking PTPRD exhibited significant learning and memory impairments.
  • Elevated microgliosis and reduced PSD95 levels were observed, indicating neuroinflammation and synaptic dysfunction.

Conclusions:

  • PTPRD deficiency exacerbates tau phosphorylation, cognitive deficits, neuroinflammation, and synaptic alterations in aging mice.
  • PTPRD is critical for maintaining tau homeostasis, potentially via the Abl1 kinase pathway.
  • PTPRD represents a potential therapeutic target for protecting against tauopathies and modulating disease progression.