Parbo, Peter, Ismail, Rola, Sommerauer, Michael, Stokholm, Morten G., Hansen, Allan K., Hansen, Kim V., Amidi, Ali, Schaldemose, Jeppe L., Gottrup, Hanne, Braendgaard, Hans, Eskildsen, Simon F., Borghammer, Per ORCID: 0000-0001-6391-8052, Hinz, Rainer ORCID: 0000-0002-7808-9207, Aanerud, Joel and Brooks, David J. (2018). Does inflammation precede tau aggregation in early Alzheimer's disease? A PET study. Neurobiol. Dis., 117. S. 211 - 217. SAN DIEGO: ACADEMIC PRESS INC ELSEVIER SCIENCE. ISSN 1095-953X

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Abstract

Objective: Our aim was to assess with positron emission tomography (PET) the temporal and spatial interrelationships between levels of cortical microglial activation and the aggregated amyloid-beta and tau load in mild cognitive impairment (MCI) and early Alzheimer's disease (AD). Methods: Six clinically probable AD and 20 MCI subjects had inflammation (C-11-(R)-PK11195), amyloid (C-11-PiB) and tau (F-18-flortaucipir) PET, magnetic resonance imaging (MRI) and a neuropsychological assessment. Parametric images of tracer binding were interrogated at a voxel level and by region of interest analyses. Results: 55% of MCI and 83% of AD subjects had a high amyloid-beta load. We have previously reported that clusters of correlated amyloid and inflammation levels are present in cortex. Here we found no correlation between levels of inflammation (C-11-(R)-PK11195 BPND) and tau (F-18-flortaucipir SUVR) or MMSE scores in high amyloid-beta cases. Interpretation: While correlated levels of amyloid-beta and inflammation can be seen in MCI, we did not detect an association between levels of cortical tau tangles and inflammation in our series of high amyloid-P cases. High levels of inflammation could be seen in amyloid-beta positive MCI cases where F-18-flortaucipir signals were low suggesting microglial activation precedes tau tangle formation. Inflammation levels were higher in high amyloid-beta MCI than in early AD cases, compatible with it initially playing a protective role.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Parbo, PeterUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ismail, RolaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Sommerauer, MichaelUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Stokholm, Morten G.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hansen, Allan K.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hansen, Kim V.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Amidi, AliUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schaldemose, Jeppe L.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Gottrup, HanneUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Braendgaard, HansUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Eskildsen, Simon F.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Borghammer, PerUNSPECIFIEDorcid.org/0000-0001-6391-8052UNSPECIFIED
Hinz, RainerUNSPECIFIEDorcid.org/0000-0002-7808-9207UNSPECIFIED
Aanerud, JoelUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Brooks, David J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-173840
DOI: 10.1016/j.nbd.2018.06.004
Journal or Publication Title: Neurobiol. Dis.
Volume: 117
Page Range: S. 211 - 217
Date: 2018
Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE
Place of Publication: SAN DIEGO
ISSN: 1095-953X
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
MILD COGNITIVE IMPAIRMENT; AMYLOID-BETA PATHOLOGY; MICROGLIAL ACTIVATION; HUMAN BRAIN; COMPOUND-B; NEUROINFLAMMATION; DEMENTIA; MODELMultiple languages
NeurosciencesMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/17384

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