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Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
07:18

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Pathological relationships between microglial cell activity and tau and amyloid beta protein in patients with

A Hayes1, U Thaker, T Iwatsubo

  • 1Clinical Neuroscience Research Group, Department of Medicine, University of Manchester, Manchester, M13 9PT, UK.

Neuroscience Letters
|October 18, 2002
PubMed

Insights

Microglial cell activation in Alzheimer's disease (AD) correlates with pathological tau, not amyloid beta. This suggests that microglial cells may contribute to neurofibrillary damage in AD by releasing toxic molecules.

Area of Science:

  • Neuroscience
  • Neuropathology
  • Immunology

Background:

  • Alzheimer's disease (AD) is characterized by the accumulation of amyloid beta (Abeta) and tau proteins.
  • Microglial cells are the primary immune cells in the brain and their activation is observed in AD.
  • The precise role of microglial activation in AD pathogenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the correlation between microglial cell activation and the load of pathological tau and Abeta proteins in Alzheimer's disease.
  • To determine if microglial cell load is associated with clinical parameters like age at onset or disease duration.

Main Methods:

  • Image analysis of ferritin-immunostained frontal cortex sections from 72 Alzheimer's disease patients.
  • Quantification of microglial cell load.
  • Correlation analysis with pathological tau and Abeta (Abeta40, Abeta42) load in adjacent sections.

Main Results:

  • Microglial cell load did not correlate with Abeta40 or Abeta42 load.
  • Microglial cell load was significantly correlated with pathological tau load.
  • Microglial cell load was unrelated to age at onset or duration of illness.

Conclusions:

  • Microglial activation in Alzheimer's disease is linked to pathological tau accumulation, not amyloid beta.
  • The findings suggest that microglial cells may precede tau pathology and contribute to neurofibrillary damage through the release of inflammatory molecules.

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