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Astrocytic tau pathologies in aged human brain.

Koichi Okamoto1, Masakuni Amari1, Toshio Fukuda2

  • 1Department of Neurology, Geriatrics Research Institute and Hospital, Maebashi, Japan.

Neuropathology : Official Journal of the Japanese Society of Neuropathology
|April 3, 2019
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Summary

Aging-related tau astrogliopathy (ARTAG) involves abnormal tau structures in astrocytes. This study found thorn-shaped astrocytes (TSA) and granular/fuzzy astrocytes (GFA) predominantly contain 4-repeat tau, not 3-repeat tau.

Keywords:
4-repeat tauARTAGastrocytepathologytau

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Aging Research

Background:

  • Aging-related tau astrogliopathy (ARTAG) is characterized by tau-positive structures in astrocytes.
  • ARTAG presents with two main morphologies: thorn-shaped astrocytes (TSA) and granular or fuzzy astrocytic processes (GFA).

Purpose of the Study:

  • To investigate the specific tau-repeat profiles (3-repeat vs. 4-repeat) within different ARTAG morphologies.
  • To characterize the distribution and composition of tau pathology in astrocytes in aged brains.

Main Methods:

  • Analysis of 28 autopsied cases with significant astrocytic tauopathy from 330 routine aged brains.
  • Immunohistochemistry using AT8 antibody and Gallyas silver staining.
  • Tau-repeat immunohistochemistry (3R-tau and 4R-tau specific antibodies).

Main Results:

  • Thorn-shaped astrocytes (TSA) were consistently positive for 4-repeat (4R) tau and negative for 3-repeat (3R) tau.
  • Granular/fuzzy astrocytic processes (GFA) in gray matter were also 4R-tau positive and 3R-tau negative.
  • 3R-tau positive structures, likely neuropil threads, were observed in subpial and subependymal areas, distinct from TSA and GFA.
  • No astrocytes co-expressing both 3R-tau and 4R-tau, or only 3R-tau, were identified.

Conclusions:

  • ARTAG, including TSA and GFA, is primarily associated with 4-repeat tau pathology.
  • The distinct tau-repeat profiles suggest different origins or pathways for tau accumulation in astrocytes versus neuronal elements.
  • Further research is required to fully elucidate the nature and progression of glial tau pathology in ARTAG.