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Lookup NU author(s): Dr Michael FirbankORCiD, Dr Rachael LawsonORCiD, Professor Alison Yarnall, Dr Gordon Duncan, Dr Tien Kheng Khoo, Professor David BrooksORCiD, Professor David Burn, Professor John O'Brien
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2017 The Authors We investigated whole-brain atrophy and ventricular enlargement over 18 months in nondemented Parkinson's disease (PD) and examined their associations with clinical measures and baseline CSF markers. PD subjects (n = 100) were classified at baseline into those with mild cognitive impairment (MCI; PD-MCI, n = 36) and no cognitive impairment (PD-NC, n = 64). Percentage of whole-brain volume change (PBVC) and ventricular expansion over 18 months were assessed with FSL-SIENA and ventricular enlargement (VIENA) respectively. PD-MCI showed increased global atrophy (−1.1% ± 0.8%) and ventricular enlargement (6.9 % ± 5.2%) compared with both PD-NC (PBVC: −0.4 ± 0.5, p < 0.01; VIENA: 2.1% ± 4.3%, p < 0.01) and healthy controls. In a subset of 35 PD subjects, CSF levels of tau, and Aβ42/Aβ40 ratio were correlated with PBVC and ventricular enlargement respectively. The sample size required to demonstrate a 20% reduction in PBVC and VIENA was approximately 1/15th of that required to detect equivalent changes in cognitive decline. These findings suggest that longitudinal MRI measurements have potential to serve as surrogate markers to complement clinical assessments for future disease-modifying trials in PD.
Author(s): Mak E, Su L, Williams GB, Firbank MJ, Lawson RA, Yarnall AJ, Duncan GW, Mollenhauer B, Owen AM, Khoo TK, Brooks DJ, Rowe JB, Barker RA, Burn DJ, O'Brien JT
Publication type: Article
Publication status: Published
Journal: Neurobiology of Aging
Year: 2017
Volume: 55
Pages: 78-90
Print publication date: 01/07/2017
Online publication date: 16/03/2017
Acceptance date: 08/03/2017
Date deposited: 02/05/2017
ISSN (print): 0197-4580
ISSN (electronic): 1558-1497
Publisher: Elsevier
URL: https://doi.org/10.1016/j.neurobiolaging.2017.03.012
DOI: 10.1016/j.neurobiolaging.2017.03.012
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