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Compared to normals, the cerebral expression of multiple inflammatory markers is reduced in Alzheimer’s disease and Diffuse Lewy body disease

Published online by Cambridge University Press:  10 December 2015

AC Lamport ,
J Warford  and
AS Easton
AC Lamport
Affiliation:
Department of Pathology, Dalhousie University, Halifax, NS
J Warford
Affiliation:
Department of Pathology, Dalhousie University, Halifax, NS
AS Easton
Affiliation:
Department of Pathology, Dalhousie University, Halifax, NS
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Abstract

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Canadian Journal of Neurological Sciences , Volume 42 , Issue S3: ABSTRACTS: 55th Annual Canadian Association of Neuropathologists Meeting , December 2015 , pp. S3
Copyright
Copyright © The Canadian Journal of Neurological Sciences Inc. 2015 

The role of inflammation in the development of dementia is a controversial topic. However, inflammatory biomarkers could be used to differentiate different subtypes of dementia, and monitor responses to therapy. Here we describe the results of a multi-plexed ELISA study using Bio-Plex Pro™ premixed 40-plex human cytokine kits to obtain an overview of inflammatory biomarker expression in the left frontal pole frozen at autopsy in pathologically verified cases of Alzheimer degeneration (Braak stage≤3), AD (Braak stage≥4), AD-DLBD (Braak stage≤3), ‘pure’ DLBD (without AD pathology) and normal controls.

Compared to normals, significant reductions were observed in levels of Interleukin (IL)-6, Tumor Necrosis Factor, IL-1β, and 5 CXCL (-2, -6, -11, -13, -16) and 4 CCL (-7, -15, -23, -26) chemokines in all cases. These reductions occurred in a stepwise fashion, with highest levels in cases of AD, followed by AD-DLBD, DLBD and Alzheimer degeneration. This suggests that inflammatory biomarkers reduce in the transition to AD, and undergo further profound reductions in cases of mixed AD-DLBD and particularly in cases of ‘pure’ DLBD. These results challenge the notion that dementia is characterized by increased brain inflammation, and suggest that biomarker reductions could be used to signal the onset of Alzheimer’s disease, while sustained biomarkers during therapy could reflect neuroprotection.

Conflictsof Interest:

None.