Imperial College London
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Professor Paul Edison

Faculty of Medicine, Department of Brain Sciences

Professor of Neuroscience
 
 
 
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Contact

 

paul.edison

 
 
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Location

 

2S 5A, Level 2Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Edison:2018:brain/awy188,
author = {Edison, P and Dani, M and wood, M and Ruth, M and Fan, Z and Walker, Z and Morgan, R and Hinz, R and Biju, M and Kuruvilla, T and Brooks, D and Edison, P},
doi = {brain/awy188},
journal = {Brain},
pages = {2740--2754},
title = {Microglial activation correlates in vivo with both tau and amyloid in Alzheimer’s disease},
url = {http://dx.doi.org/10.1093/brain/awy188},
volume = {141},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Alzheimer’s disease is characterized by the histopathological presence of amyloid-β plaques and tau-containing neurofibrillary tangles. Microglial activation is also a recognized pathological component. The relationship between microglial activation and protein aggregation is still debated. We investigated the relationship between amyloid plaques, tau tangles and activated microglia using PET imaging. Fifty-one subjects (19 healthy controls, 16 mild cognitive impairment and 16 Alzheimer’s disease subjects) participated in the study. All subjects had neuropsychometric testing, MRI, amyloid (18F-flutemetamol), and microglial (11C-PBR28) PET. All subjects with mild cognitive impairment and Alzheimer’s disease and eight of the controls had tau (18F-AV1451) PET. 11C-PBR28 PET was analysed using Logan graphical analysis with an arterial plasma input function, while 18F-flutemetamol and 18F-AV1451 PET were analysed as target:cerebellar ratios to create parametric standardized uptake value ratio maps. Biological parametric mapping in the Statistical Parametric Mapping platform was used to examine correlations between uptake of tracers at a voxel-level. There were significant widespread clusters of positive correlation between levels of microglial activation and tau aggregation in both the mild cognitive impairment (amyloid-positive and amyloid-negative) and Alzheimer’s disease subjects. The correlations were stronger in Alzheimer’s disease than in mild cognitive impairment, suggesting that these pathologies increase together as disease progresses. Levels of microglial activation and amyloid deposition were also correlated, although in a different spatial distribution; correlations were stronger in mild cognitive impairment than Alzheimer’s subjects, in line with a plateauing of amyloid load with disease progression. Clusters of positive correlations between microglial activation and protein aggregation often targeted similar areas of
AU  - Edison,P
AU  - Dani,M
AU  - wood,M
AU  - Ruth,M
AU  - Fan,Z
AU  - Walker,Z
AU  - Morgan,R
AU  - Hinz,R
AU  - Biju,M
AU  - Kuruvilla,T
AU  - Brooks,D
AU  - Edison,P
DO  - brain/awy188
EP  - 2754
PY  - 2018///
SN  - 1460-2156
SP  - 2740
TI  - Microglial activation correlates in vivo with both tau and amyloid in Alzheimer’s disease
T2  - Brain
UR  - http://dx.doi.org/10.1093/brain/awy188
UR  - http://hdl.handle.net/10044/1/81184
VL  - 141
ER  -
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