Supplementary Material for: Patterns of Microglial Cell Activation in Alzheimer Disease and Frontotemporal Lobar Degeneration

  • Ricardo Taipa (Centro Hospitalar do Porto) (Contributor)
  • Paulo Brochado (Contributor)
  • Andrew Robinson (Contributor)
  • Inês Reis (Contributor)
  • Patrício Costa (Contributor)
  • David Mann (Contributor)
  • Manuel Melo Pires (Contributor)
  • Nuno Sousa (Contributor)



<p><b><i>Aims:</i></b> Microglia-driven neuroinflammation can play an
important role in the pathophysiology of neurodegenerative disorders. In
this study, we sought to characterize the distribution of microglial
cell activation in 2 neurodegenerative dementias with distinct protein
signatures, Alzheimer disease (AD) and frontotemporal lobar degeneration
(FTLD) of the TDP subtype, and to determine if there was an anatomical
correlation with the phenotypes most commonly associated with these
conditions. <b><i>Methods:</i></b> The distribution and extent of
microglial cell activation was assessed semiquantitatively in the
hippocampal formation, cortical gray matter, and subcortical white
matter of CD68-immunostained sections of the frontal, temporal,
parietal, and occipital cortices from 15 pathologically confirmed cases
of AD, 13 cases of FTLD, and 18 controls. <b><i>Results:</i></b>
Significantly higher levels of microglial cell activation occurred in
the subiculum in AD and FTLD than in controls. Additionally, AD had
higher microglial activation in the CA1 and FTLD in the hippocampal
white matter than the controls. Microglial activation was greater in the
dentate gyrus molecular layer in AD than in FTLD. In the cortical
regions, the 2 pathological groups differed only in frontal white
matter, with the FTLD group showing higher microglial scores. FTLD
showed higher microglial activation in the white matter compared to the
respective gray matter in the entorhinal, temporal, and frontal regions.
<b><i>Conclusions:</i></b> Our work expands the knowledge of the
distribution and magnitude of microglial activation in these disorders.
Additionally, we found some microglial circuit-specific patterns that
could help to explain some of the clinical overlap between AD and
FTLD-TDP, namely in memory deficits.</p>
Date made available26 Apr 2017

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