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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Complement dysregulation in human tauopathies.

Jacqui Nimmo1, Samuel Keat1, Louis De Muynck2

  • 1UK Dementia Research Institute Cardiff, Cardiff University, Cardiff, UK.

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|May 27, 2025
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Summary
This summary is machine-generated.

Complement activation occurs on neurons in human tauopathies like Pick's disease, globular glial tauopathy, and corticobasal degeneration. This study reveals complement's role in tau-related neurodegeneration and demyelination.

Keywords:
complementfrontotemporal dementiainflammationmyelintautauopathy

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Complement system dysregulation contributes to neurodegenerative diseases like Alzheimer's disease (AD).
  • While complement's role in amyloid pathology is studied, its involvement in human tauopathies is largely unknown.
  • Tau pathology, independent of amyloid, drives neuronal loss in AD and primary tauopathies.

Purpose of the Study:

  • To investigate complement activation in human tauopathy subtypes: Pick's disease (PiD), globular glial tauopathy (GGT), and corticobasal degeneration (CBD).
  • To determine if complement activation occurs on neurons and other brain structures in these tauopathies.

Main Methods:

  • Immunohistochemistry was used to assess complement components (C1q, iC3b, TCC) in post-mortem brain tissue from tauopathy cases and controls.
  • ELISA measured complement proteins, regulators, and activation products in brain homogenates.
  • Three tauopathy subtypes (PiD, GGT, CBD) were analyzed.

Main Results:

  • Complement activation markers (C1q, iC3b, TCC) were elevated in all tauopathy subtypes compared to controls.
  • Complement deposition (C1q, C3b/iC3b) was prominent on neurons across all tauopathies.
  • Significant increases in TCC were observed in CBD and GGT.
  • Unique to GGT, C3b/iC3b deposition on myelin suggests complement involvement in demyelination.
  • ELISA confirmed elevated C3b/iC3b, Ba, and Factor I in CBD and GGT.

Conclusions:

  • Complement is activated on and adjacent to neurons in human tauopathies.
  • These findings highlight the complement system's role in the pathogenesis of diverse tauopathies.
  • Complement may contribute to neuronal damage and demyelination in specific tauopathies like GGT.