Longitudinal changes of cortical microstructure in Parkinson's disease assessed with T1 relaxometry
Language English Country Netherlands Media electronic-ecollection
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
J-0901
Parkinson's UK - United Kingdom
PubMed
28116233
PubMed Central
PMC5226811
DOI
10.1016/j.nicl.2016.12.025
PII: S2213-1582(16)30262-5
Knihovny.cz E-resources
- Keywords
- BG, basal ganglia, Cerebral cortex, GE, gradient echo, GM, gray matter, HY, Hoehn and Yahr, Longitudinal, MRI, magnetic resonance imaging, PD, Parkinson's disease, Parkinson's disease, Quantitative MRI, Relaxometry, SN, substantia nigra, T1, UPDRS III, motor part of the Unified Parkinson's disease rating scale, qMRI, quantitative MRI,
- MeSH
- Middle Aged MeSH
- Humans MeSH
- Longitudinal Studies MeSH
- Magnetic Resonance Imaging methods MeSH
- Cerebral Cortex diagnostic imaging MeSH
- Parkinson Disease diagnostic imaging MeSH
- Aged MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: Histological evidence suggests that pathology in Parkinson's disease (PD) goes beyond nigrostriatal degeneration and also affects the cerebral cortex. Quantitative MRI (qMRI) techniques allow the assessment of changes in brain tissue composition. However, the development and pattern of disease-related cortical changes have not yet been demonstrated in PD with qMRI methods. The aim of this study was to investigate longitudinal cortical microstructural changes in PD with quantitative T1 relaxometry. METHODS: 13 patients with mild to moderate PD and 20 matched healthy subjects underwent high resolution T1 mapping at two time points with an interval of 6.4 years (healthy subjects: 6.5 years). Data from two healthy subjects had to be excluded due to MRI artifacts. Surface-based analysis of cortical T1 values was performed with the FreeSurfer toolbox. RESULTS: In PD patients, a widespread decrease of cortical T1 was detected during follow-up which affected large parts of the temporo-parietal and occipital cortices and also frontal areas. In contrast, age-related T1 decrease in the healthy control group was much less pronounced and only found in lateral frontal, parietal and temporal areas. Average cortical T1 values did not differ between the groups at baseline (p = 0.17), but were reduced in patients at follow-up (p = 0.0004). Annualized relative changes of cortical T1 were higher in patients vs. healthy subjects (patients: - 0.72 ± 0.64%/year; healthy subjects: - 0.17 ± 0.41%/year, p = 0.007). CONCLUSIONS: In patients with PD, the development of widespread changes in cortical microstructure was observed as reflected by a reduction of cortical T1. The pattern of T1 decrease in PD patients exceeded the normal T1 decrease as found in physiological aging and showed considerable overlap with the pattern of cortical thinning demonstrated in previous PD studies. Therefore, cortical T1 might be a promising additional imaging marker for future longitudinal PD studies. The biological mechanisms underlying cortical T1 reductions remain to be further elucidated.
Brain Imaging Center Goethe University Frankfurt Main Germany
Department of Neurology Goethe University Frankfurt Main Germany
Dr Senckenberg Chronomedical Institute Goethe University Frankfurt Main Germany
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