Imperial College London
Alternate

ProfessorDavidDexter

Faculty of Medicine, Department of Brain Sciences

Visiting Professor of Neuropharmacology
 
 
 
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Contact

 

+44 (0)20 7594 6665d.dexter Website

 
 
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Location

 

E411Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Ruffmann:2015:10.1111/nan.12294,
author = {Ruffmann, C and Calboli, FC and Bravi, I and Gveric, D and Curry, LK and de, Smith A and Pavlou, S and Buxton, JL and Blakemore, AI and Takousis, P and Molloy, S and Piccini, P and Dexter, DT and Roncaroli, F and Gentleman, SM and Middleton, LT},
doi = {10.1111/nan.12294},
journal = {Neuropathology and Applied Neurobiology},
pages = {436--450},
title = {Cortical Lewy bodies and Aβ burden are associated with prevalence and timing of dementia in Lewy body diseases.},
url = {http://dx.doi.org/10.1111/nan.12294},
volume = {42},
year = {2015}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - AIMS: Our main objective was to determine the neuropathological correlates of dementia in patients with Lewy body disease (LBD). Furthermore, we used data derived from clinical, neuropathological and genetic studies to investigate boundary issues between Dementia with Lewy bodies (DLB) and Parkinson's disease with (PDD) and without (PDND) dementia. METHODS: 121 cases with a neuropathological diagnosis of LBD and clinical information on dementia status were included in the analysis (55 PDD, 17 DLB and 49 PDND). We carried out topographical and semi-quantitative assessment of Lewy bodies (LB), Aβ plaques and tau-positive neuropil threads (NT). The APOE genotype and MAPT haplotype status were also determined. RESULTS: The cortical LB (CLB) burden was the only independent predictor of dementia (OR: 4.12, p<0.001). The total cortical Aβ plaque burden was an independent predictor of a shorter latency to dementia from onset of motor signs (p=0.001). DLB cases had a higher LB burden in the parietal and temporal cortex, compared to PDD. Carrying at least one APOE 4 allele was associated with a higher cortical LB burden (p=0.02), particularly in the neocortical frontal, parietal, and temporal regions. CONCLUSIONS: High CLB burden is a key neuropathological substrate of dementia in LBD. Elevated cortical LB pathology and Aβ plaque deposition are both correlated with a faster progression to dementia. The higher CLB load in the temporal and parietal regions, which seems to be a distinguishing feature of DLB, may account for the shorter latency to dementia and could be mediated by the APOE 4 allele. This article is protected by copyright. All rights reserved.
AU  - Ruffmann,C
AU  - Calboli,FC
AU  - Bravi,I
AU  - Gveric,D
AU  - Curry,LK
AU  - de,Smith A
AU  - Pavlou,S
AU  - Buxton,JL
AU  - Blakemore,AI
AU  - Takousis,P
AU  - Molloy,S
AU  - Piccini,P
AU  - Dexter,DT
AU  - Roncaroli,F
AU  - Gentleman,SM
AU  - Middleton,LT
DO  - 10.1111/nan.12294
EP  - 450
PY  - 2015///
SN  - 1365-2990
SP  - 436
TI  - Cortical Lewy bodies and Aβ burden are associated with prevalence and timing of dementia in Lewy body diseases.
T2  - Neuropathology and Applied Neurobiology
UR  - http://dx.doi.org/10.1111/nan.12294
UR  - http://hdl.handle.net/10044/1/30027
VL  - 42
ER  -
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