Journal
BRAIN
Volume 140, Issue -, Pages 2002-2011Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/awx120
Keywords
Alzheimer's disease; mild cognitive impairment; microglial activation; beta-amyloid; positron emission tomography
Categories
Funding
- Danish Council for Independent Research
- Lundbeck Foundation
- Medical Research Council
- Higher Education Funding Council for England (HEFCE)
- Alzheimer's Research, UK
- Alzheimer's Drug Discovery Foundation
- Alzheimer's Society, UK
- Novo Nordisk
- Piramal Life Science
- GE Healthcare
- European Union [HEALTH-F2-2011-278850]
- Alzheimer's Research Trust
- Michael J Fox foundation
- European Commission
- MRC [G84/6523] Funding Source: UKRI
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Subjects with mild cognitive impairment associated with cortical amyloid-beta have a greatly increased risk of progressing to Alzheimer's disease. We hypothesized that neuroinflammation occurs early in Alzheimer's disease and would be present in most amyloid-positive mild cognitive impairment cases. C-11-Pittsburgh compound B and C-11-(R)-PK11195 positron emission tomography was used to determine the amyloid load and detect the extent of neuroinflammation (microglial activation) in 42 mild cognitive impairment cases. Twelve age-matched healthy control subjects had C-11-Pittsburgh compound B and 10 healthy control subjects had C-11-(R)-PK11195 positron emission tomography for comparison. Amyloid-positivity was defined as C-11-Pittsburgh compound B target-to-cerebellar ratio above 1.5 within a composite cortical volume of interest. Supervised cluster analysis was used to generate parametric maps of C-11-(R)-PK11195 binding potential. Levels of C-11-(R)-PK11195 binding potential were measured in a selection of cortical volumes of interest and at a voxel level. Twenty-six (62%) of 42 mild cognitive impairment cases showed a raised cortical amyloid load compared to healthy controls. Twenty-two (85%) of the 26 amyloid-positive mild cognitive impairment cases showed clusters of increased cortical microglial activation accompanying the amyloid. There was a positive correlation between levels of amyloid load and C-11-(R)-PK11195 binding potentials at a voxel level within subregions of frontal, parietal and temporal cortices. C-11-(R)-PK11195 positron emission tomography reveals increased inflammation in a majority of amyloid positive mild cognitive impairment cases, its cortical distribution overlapping that of amyloid deposition.
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