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Globular glial tauopathy type II
  1. Patrick W Cullinane1,2,
  2. Katie Sidle3,
  3. Kailash P Bhatia1,
  4. Tamas Revesz2,4,
  5. Thomas T Warner1,2
  1. 1Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, UK
  2. 2Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, London, UK
  3. 3Department of Neuromuscular Disease, UCL Queen Square Institute of Neurology, London, UK
  4. 4Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK
  1. Correspondence to Professor Thomas T Warner, Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK; t.warner{at}ucl.ac.uk

Abstract

The globular glial tauopathies (GGTs) are a rare group of neurodegenerative diseases with fewer than 90 autopsy-confirmed cases reported in the literature. Although there has been some uncertainty about whether GGT is entirely distinct from progressive supranuclear palsy, a recent study of tau filament structures supports the definition of GGT as a separate neuropathological entity. We present a sporadic case of GGT type II presenting with a progressive corticobasal–primary lateral sclerosis overlap syndrome in a 74-year-old woman. Neuropathological examination identified neuronal and glial tau inclusions, including globular astrocytic and oligodendroglial inclusions. We also discuss the clinical features and molecular pathophysiology of GGT. Increased awareness of this condition could become more important as patients with GGT may be candidates for anti-tau therapies currently undergoing clinical evaluation in patients with other tauopathies.

  • NEUROPATHOLOGY

Data availability statement

Data sharing not applicable as no datasets generated and/or analysed for this study.

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Data availability statement

Data sharing not applicable as no datasets generated and/or analysed for this study.

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Footnotes

  • Contributors PWC and TR drafted the manuscript and KS, KPB and TTW revised the manuscript and provided important intellectual content.

  • Funding PWC is supported by funding from the Reta Lila Weston Trust for Medical Research.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed by Richard Davenport, Edinburgh, UK.

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