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Neurobiol Aging. 2017 Jul;55:78-90. doi: 10.1016/j.neurobiolaging.2017.03.012. Epub 2017 Mar 16.

Longitudinal whole-brain atrophy and ventricular enlargement in nondemented Parkinson's disease.

Author information

1
Department of Psychiatry, University of Cambridge, Cambridgeshire, UK.
2
Wolfson Brain Imaging Centre, University of Cambridge, Cambridgeshire, UK.
3
Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK.
4
Medicine of the Elderly, Western General Hospital, Edinburgh, UK.
5
Paracelsus-Elena-Klinik, Kassel, Germany; University Medical Center Goettingen, Institute of Neuropathology, Goettingen, Germany.
6
Brain and Mind Institute, University of Western Ontario, London, Canada; Department of Psychology, University of Western Ontario, London, Canada.
7
Menzies Health Institute, Queensland and School of Medicine, Griffith University, Gold Coast, Australia.
8
Division of Neuroscience, Imperial College London, London, UK; Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark.
9
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.
10
John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.
11
Department of Psychiatry, University of Cambridge, Cambridgeshire, UK. Electronic address: John.obrien@medschl.cam.ac.uk.

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

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