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Longitudinal whole-brain atrophy and ventricular enlargement in nondemented Parkinsons disease


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Publication Date: 2017-07-01

Journal Title: Neurobiology of Aging

Publisher: Elsevier BV

Volume: 55

Pages: 78-90

Language: English

Type: Article

This Version: VoR

Metadata: Show full item record

Citation: Mak, E., Su, L., Williams, G., Firbank, M., Lawson, R., Yarnall, A., Duncan, G., et al. (2017). Longitudinal whole-brain atrophy and ventricular enlargement in nondemented Parkinson's disease. Neurobiology of Aging, 55 78-90. https://doi.org/10.1016/j.neurobiolaging.2017.03.012

Abstract: 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.

Keywords: dementia, imaging, longitudinal, MRI, neurodegeneration, Parkinson's disease

Sponsorship: This study was funded by a Parkinson's UK grant (J-0802) and supported by Parkinson's UK (CN), Lockhart Parkinson's Disease Research Fund (RAL, TKK, GWD), Michael J. Fox Foundation (AJY), the National Institute for Health Research (NIHR, RG64473) Cambridge Biomedical Research Centre, and Biomedical Research Unit in Dementia, the Wellcome Trust (JBR, 103838); the Medical Research Council of Cognition, and Brain Sciences Unit, Cambridge (JBR, MC-A060-5PQ30); the NIHR Newcastle Biomedical Research Unit based at Newcastle-upon-Tyne Hospitals NHS Foundation Trust and Newcastle University; the NIHR Dementia and Neurodegenerative Diseases Research Network (JTO), and Elijah Mak was in receipt of the Gates Cambridge studentship and Alzheimer's Research UK scholarship.

Embargo Lift Date: 2100-01-01

Identifiers:

External DOI: https://doi.org/10.1016/j.neurobiolaging.2017.03.012

This record's URL: https://www.repository.cam.ac.uk/handle/1810/264452



Rights: Attribution 4.0 International

Licence URL: http://creativecommons.org/licenses/by/4.0/





Autor: Mak, ESu, LWilliams, GBFirbank, MJLawson, RAYarnall, AJDuncan, GWMollenhauer, BOwen, AMKhoo, TKBrooks, DJ Rowe, JB Barker, RABurn,

Fuente: https://www.repository.cam.ac.uk/handle/1810/264452



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