Torben Ellegaard Lund

Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer's disease

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Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer's disease. / Parbo, Peter; Ismail, Rola; Hansen, Kim V; Amidi, Ali; Mårup, Frederik H; Gottrup, Hanne; Brændgaard, Hans; Eriksson, Bengt Olof Mikael; Eskildsen, Simon F; Lund, Torben E; Tietze, Anna; Edison, Paul; Pavese, Nicola; Stokholm, Morten G; Borghammer, Per; Hinz, Rainer; Aanerud, Joel; Brooks, David J.

In: Brain, Vol. 140, No. 7, 01.07.2017, p. 2002-2011.

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@article{076abbb0e0194e13a0f35e5fdca3a0a5,
title = "Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer's disease",
abstract = "Subjects with mild cognitive impairment associated with cortical amyloid-β 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. 11C-Pittsburgh compound B and 11C-(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 11C-Pittsburgh compound B and 10 healthy control subjects had 11C-(R)-PK11195 positron emission tomography for comparison. Amyloid-positivity was defined as 11C-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 11C-(R)-PK11195 binding potential. Levels of 11C-(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 11C-(R)-PK11195 binding potentials at a voxel level within subregions of frontal, parietal and temporal cortices. 11C-(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.",
keywords = "Journal Article",
author = "Peter Parbo and Rola Ismail and Hansen, {Kim V} and Ali Amidi and M{\aa}rup, {Frederik H} and Hanne Gottrup and Hans Br{\ae}ndgaard and Eriksson, {Bengt Olof Mikael} and Eskildsen, {Simon F} and Lund, {Torben E} and Anna Tietze and Paul Edison and Nicola Pavese and Stokholm, {Morten G} and Per Borghammer and Rainer Hinz and Joel Aanerud and Brooks, {David J}",
note = "{\textcopyright} The Author (2017). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.",
year = "2017",
month = jul,
day = "1",
doi = "10.1093/brain/awx120",
language = "English",
volume = "140",
pages = "2002--2011",
journal = "Brain",
issn = "0006-8950",
publisher = "Oxford University Press",
number = "7",

}

RIS

TY - JOUR

T1 - Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer's disease

AU - Parbo, Peter

AU - Ismail, Rola

AU - Hansen, Kim V

AU - Amidi, Ali

AU - Mårup, Frederik H

AU - Gottrup, Hanne

AU - Brændgaard, Hans

AU - Eriksson, Bengt Olof Mikael

AU - Eskildsen, Simon F

AU - Lund, Torben E

AU - Tietze, Anna

AU - Edison, Paul

AU - Pavese, Nicola

AU - Stokholm, Morten G

AU - Borghammer, Per

AU - Hinz, Rainer

AU - Aanerud, Joel

AU - Brooks, David J

N1 - © The Author (2017). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

PY - 2017/7/1

Y1 - 2017/7/1

N2 - Subjects with mild cognitive impairment associated with cortical amyloid-β 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. 11C-Pittsburgh compound B and 11C-(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 11C-Pittsburgh compound B and 10 healthy control subjects had 11C-(R)-PK11195 positron emission tomography for comparison. Amyloid-positivity was defined as 11C-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 11C-(R)-PK11195 binding potential. Levels of 11C-(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 11C-(R)-PK11195 binding potentials at a voxel level within subregions of frontal, parietal and temporal cortices. 11C-(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.

AB - Subjects with mild cognitive impairment associated with cortical amyloid-β 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. 11C-Pittsburgh compound B and 11C-(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 11C-Pittsburgh compound B and 10 healthy control subjects had 11C-(R)-PK11195 positron emission tomography for comparison. Amyloid-positivity was defined as 11C-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 11C-(R)-PK11195 binding potential. Levels of 11C-(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 11C-(R)-PK11195 binding potentials at a voxel level within subregions of frontal, parietal and temporal cortices. 11C-(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.

KW - Journal Article

U2 - 10.1093/brain/awx120

DO - 10.1093/brain/awx120

M3 - Journal article

C2 - 28575151

VL - 140

SP - 2002

EP - 2011

JO - Brain

JF - Brain

SN - 0006-8950

IS - 7

ER -