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Patterns of microglial cell activation in frontotemporal lobar degeneration
Author(s) -
Lant Suzannah B.,
Robinson Andrew C.,
Thompson Jennifer C.,
Rollinson Sara,
PickeringBrown Stuart,
Snowden Julie S.,
Davidson Yvonne S.,
Gerhard Alexander,
Mann David M. A.
Publication year - 2014
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12092
Subject(s) - frontotemporal lobar degeneration , grey matter , white matter , pathology , temporal lobe , temporal cortex , microglia , frontal lobe , biology , pathological , neuroscience , frontotemporal dementia , medicine , magnetic resonance imaging , disease , dementia , epilepsy , inflammation , immunology , radiology
Aims Pathological heterogeneity within patients with frontotemporal lobar degeneration ( FTLD ) 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 FTLD in order to determine whether it might be possible to employ this as a diagnostic marker in vivo using PET ligand [11 C ]( R )‐ PK 11195 in order to differentiate cases of FTLD according to histological subtype. Methods The distribution and extent of microglial cell activation was assessed semi‐quantitatively in cortical grey and subcortical white matter of CD 68 immunostained sections of frontal and temporal cortex from 78 pathologically confirmed cases of FTLD , 13 of A lzheimer's disease ( AD ) and 13 controls. Results Significantly higher levels of microglial cell activation than controls occurred in all four regions in FTLD , and in three of the four regions in AD . Microglial activation was greater in frontal subcortical white matter in FTLD than AD , whereas it was higher in temporal cortical grey matter in AD than FTLD . Microglial cell activation was significantly higher in temporal subcortical white matter in FTLD‐ MAPT than in other genetic ( GRN , C9ORF 72 ) or non‐genetic forms of FTLD . Conclusions The present study suggests that high levels of microglial cell involvement in temporal lobe (subcortical white matter) might serve as a marker of inherited FTLD associated with intronic mutations in MAPT , with a relatively intense signal in this region in PET studies using [11 C ]( R )‐ PK 11195 as microglial cell marker could indicate the presence of MAPT mutation in vivo .