> Details

Lant, Suzannah B.; Robinson, Andrew C.; Thompson, Jennifer C.; Rollinson, Sara; Pickering‐Brown, Stuart; Snowden, Julie S.; Davidson, Yvonne S.; Gerhard, Alexander; Mann, David M. A.

Patterns of microglial cell activation in frontotemporal lobar degeneration

Reference
management

Bookmarks

Remove from
bookmarks

Share this on Whatsapp

Close

Bookmarks



You can manage bookmarks using lists, please log in to your user account for this.
  • Media type: E-Article
  • Title: Patterns of microglial cell activation in frontotemporal lobar degeneration
  • Contributor: Lant, Suzannah B.; Robinson, Andrew C.; Thompson, Jennifer C.; Rollinson, Sara; Pickering‐Brown, Stuart; Snowden, Julie S.; Davidson, Yvonne S.; Gerhard, Alexander; Mann, David M. A.
  • Published: Wiley, 2014
  • Published in: Neuropathology and Applied Neurobiology, 40 (2014) 6, Seite 686-696
  • Language: English
  • DOI: 10.1111/nan.12092
  • ISSN: 0305-1846; 1365-2990
  • Origination:
  • Footnote:
  • Description: <jats:sec><jats:title>Aims</jats:title><jats:p>Pathological heterogeneity within patients with frontotemporal lobar degeneration (<jats:styled-content style="fixed-case">FTLD</jats:styled-content>) in general precludes the accurate assignment of diagnostic subtype in life. The aim of this study was to assess the extent of microglial cell activation in <jats:styled-content style="fixed-case">FTLD</jats:styled-content> in order to determine whether it might be possible to employ this as a diagnostic marker <jats:italic>in vivo</jats:italic> using <jats:styled-content style="fixed-case">PET</jats:styled-content> ligand [11<jats:styled-content style="fixed-case">C</jats:styled-content>](<jats:styled-content style="fixed-case">R</jats:styled-content>)‐<jats:styled-content style="fixed-case">PK</jats:styled-content>11195 in order to differentiate cases of <jats:styled-content style="fixed-case">FTLD</jats:styled-content> according to histological subtype.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>The distribution and extent of microglial cell activation was assessed semi‐quantitatively in cortical grey and subcortical white matter of <jats:styled-content style="fixed-case">CD</jats:styled-content>68 immunostained sections of frontal and temporal cortex from 78 pathologically confirmed cases of <jats:styled-content style="fixed-case">FTLD</jats:styled-content>, 13 of <jats:styled-content style="fixed-case">A</jats:styled-content>lzheimer's disease (<jats:styled-content style="fixed-case">AD</jats:styled-content>) and 13 controls.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Significantly higher levels of microglial cell activation than controls occurred in all four regions in <jats:styled-content style="fixed-case">FTLD</jats:styled-content>, and in three of the four regions in <jats:styled-content style="fixed-case">AD</jats:styled-content>. Microglial activation was greater in frontal subcortical white matter in <jats:styled-content style="fixed-case">FTLD</jats:styled-content> than <jats:styled-content style="fixed-case">AD</jats:styled-content>, whereas it was higher in temporal cortical grey matter in <jats:styled-content style="fixed-case">AD</jats:styled-content> than <jats:styled-content style="fixed-case">FTLD</jats:styled-content>. Microglial cell activation was significantly higher in temporal subcortical white matter in <jats:styled-content style="fixed-case">FTLD‐<jats:italic>MAPT</jats:italic></jats:styled-content> than in other genetic (<jats:styled-content style="fixed-case"><jats:italic>GRN</jats:italic></jats:styled-content>, <jats:styled-content style="fixed-case"><jats:italic>C9ORF</jats:italic></jats:styled-content><jats:italic>72</jats:italic>) or non‐genetic forms of <jats:styled-content style="fixed-case">FTLD</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>The present study suggests that high levels of microglial cell involvement in temporal lobe (subcortical white matter) might serve as a marker of inherited <jats:styled-content style="fixed-case">FTLD</jats:styled-content> associated with intronic mutations in <jats:styled-content style="fixed-case"><jats:italic>MAPT</jats:italic></jats:styled-content>, with a relatively intense signal in this region in <jats:styled-content style="fixed-case">PET</jats:styled-content> studies using [11<jats:styled-content style="fixed-case">C</jats:styled-content>](<jats:styled-content style="fixed-case">R</jats:styled-content>)‐<jats:styled-content style="fixed-case">PK</jats:styled-content>11195 as microglial cell marker could indicate the presence of <jats:styled-content style="fixed-case"><jats:italic>MAPT</jats:italic></jats:styled-content> mutation<jats:italic> in vivo</jats:italic>.</jats:p></jats:sec>