scholarly journals Longitudinal changes in free-water within the substantia nigra of Parkinson’s disease

Brain ◽  
2015 ◽  
Vol 138 (8) ◽  
pp. 2322-2331 ◽  
Author(s):  
Edward Ofori ◽  
Ofer Pasternak ◽  
Peggy J. Planetta ◽  
Hong Li ◽  
Roxana G. Burciu ◽  
...  
2015 ◽  
Vol 36 (2) ◽  
pp. 1097-1104 ◽  
Author(s):  
Edward Ofori ◽  
Ofer Pasternak ◽  
Peggy J. Planetta ◽  
Roxana Burciu ◽  
Amy Snyder ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247552
Author(s):  
Krzysztof Dzieciol ◽  
Elene Iordanishvili ◽  
Zaheer Abbas ◽  
Adjmal Nahimi ◽  
Michael Winterdahl ◽  
...  

Alterations in the substantia nigra are strongly associated with Parkinson’s disease. However, due to low contrast and partial volume effects present in typical MRI images, the substantia nigra is not of sufficient size to obtain a reliable segmentation for region-of-interest based analysis. To combat this problem, the approach proposed here offers a method to investigate and reveal changes in quantitative MRI parameters in the vicinity of substantia nigra without any a priori delineation. This approach uses an alternative method of statistical, voxel-based analysis of quantitative maps and was tested on 18 patients and 15 healthy controls using a well-established, quantitative free water mapping protocol. It was possible to reveal the topology and the location of pathological changes in the substantia nigra and its vicinity. Moreover, a decrease in free water content, T1 and T2* in the vicinity of substantia nigra was indicated in the Parkinson’s disease patients compared to the healthy controls. These findings reflect a disruption of grey matter and iron accumulation, which is known to lead to neurodegeneration. Consequently, the proposed method demonstrates an increased sensitivity for the detection of pathological changes—even in small regions—and can facilitate disease monitoring via quantitative MR parameters.


2019 ◽  
Vol 65 ◽  
pp. 146-152 ◽  
Author(s):  
Germain Arribarat ◽  
Ofer Pasternak ◽  
Amaury De Barros ◽  
Monique Galitzky ◽  
Oliver Rascol ◽  
...  

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
C Funke ◽  
A Soehn ◽  
C Schulte ◽  
M Bonin ◽  
C Klein ◽  
...  

Author(s):  
Antonina Kouli ◽  
Marta Camacho ◽  
Kieren Allinson ◽  
Caroline H. Williams-Gray

AbstractParkinson’s disease dementia is neuropathologically characterized by aggregates of α-synuclein (Lewy bodies) in limbic and neocortical areas of the brain with additional involvement of Alzheimer’s disease-type pathology. Whilst immune activation is well-described in Parkinson’s disease (PD), how it links to protein aggregation and its role in PD dementia has not been explored. We hypothesized that neuroinflammatory processes are a critical contributor to the pathology of PDD. To address this hypothesis, we examined 7 brain regions at postmortem from 17 PD patients with no dementia (PDND), 11 patients with PD dementia (PDD), and 14 age and sex-matched neurologically healthy controls. Digital quantification after immunohistochemical staining showed a significant increase in the severity of α-synuclein pathology in the hippocampus, entorhinal and occipitotemporal cortex of PDD compared to PDND cases. In contrast, there was no difference in either tau or amyloid-β pathology between the groups in any of the examined regions. Importantly, we found an increase in activated microglia in the amygdala of demented PD brains compared to controls which correlated significantly with the extent of α-synuclein pathology in this region. Significant infiltration of CD4+ T lymphocytes into the brain parenchyma was commonly observed in PDND and PDD cases compared to controls, in both the substantia nigra and the amygdala. Amongst PDND/PDD cases, CD4+ T cell counts in the amygdala correlated with activated microglia, α-synuclein and tau pathology. Upregulation of the pro-inflammatory cytokine interleukin 1β was also evident in the substantia nigra as well as the frontal cortex in PDND/PDD versus controls with a concomitant upregulation in Toll-like receptor 4 (TLR4) in these regions, as well as the amygdala. The evidence presented in this study show an increased immune response in limbic and cortical brain regions, including increased microglial activation, infiltration of T lymphocytes, upregulation of pro-inflammatory cytokines and TLR gene expression, which has not been previously reported in the postmortem PDD brain.


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