Diagnostic value of brain MRI and18F-FDG PET in the differentiation of parkinsonian type multiple system atrophy from Parkinson’s disease

2008 ◽  
Vol 15 (10) ◽  
pp. 1043-1049 ◽  
Author(s):  
K.-Y. Kwon ◽  
C. G. Choi ◽  
J. S. Kim ◽  
M. C. Lee ◽  
S. J. Chung
2007 ◽  
Vol 22 (16) ◽  
pp. 2352-2358 ◽  
Author(s):  
Kyum-Yil Kwon ◽  
Choong G. Choi ◽  
Jae S. Kim ◽  
Myoung C. Lee ◽  
Sun J. Chung

2021 ◽  
Author(s):  
Xuehan Hu ◽  
Xun Sun ◽  
Fan Hu ◽  
Fang Liu ◽  
Weiwei Ruan ◽  
...  

Abstract Purpose To construct multivariate radiomics models using hybrid 18F-FDG PET/MRI for distinguishing between Parkinson’s disease (PD) and multiple system atrophy (MSA). Methods Ninety patients (60 with PD and 30 with MSA) were randomised to training and validation sets in a 7:3 ratio. All patients underwent 18F-Fluorodeoxyglucose (18F-FDG) PET/MRI to simultaneously obtain metabolic images (18F-FDG), structural MRI images (T1-weighted imaging [T1WI], T2-weighted imaging [T2WI] and T2-weighted fluid-attenuated inversion recovery [T2/flair]) and functional MRI images (susceptibility-weighted imaging [SWI] and apparent diffusion coefficient). Using PET and five MRI sequences, we extracted 1172 radiomics features from the putamina and caudate nuclei. The radiomics signatures were constructed with the least absolute shrinkage and selection operator algorithm in the training set, with progressive optimization through single-sequence and double-sequence radiomics models. ໿Multivariable logistic regression analysis was used to develop a clinical-radiomics model, combining the optimal multi-sequence radiomics signature with clinical characteristics and SUV values. The diagnostic performance of the models was assessed by receiver operating characteristic and decision curve analysis (DCA). Results The radiomics signatures showed favourable diagnostic efficacy. The optimal model comprised structural (T1WI), functional (SWI), and metabolic (18F-FDG) sequences (RadscoreFDG_T1WI_SWI) with the area under curves (AUCs) of the training and validation sets of 0.971 and 0.957, respectively. The integrated model, incorporating RadscoreFDG_T1WI_SWI, three clinical symptoms (disease duration, dysarthria and autonomic failure) and SUVmax, demonstrated satisfactory calibration and discrimination in the training and validation sets (0.993 and 0.994, respectively). DCA indicated the highest clinical benefit of the clinical-radiomics integrated model. Conclusions The radiomics signature with metabolic, structural, and functional information provided by hybrid 18F-FDG PET/MRI may achieve promising diagnostic efficacy for distinguishing between PD and MSA. The clinical-radiomics integrated model performed best. ໿


2004 ◽  
Vol 35 (03) ◽  
Author(s):  
G Wasner ◽  
P Remien ◽  
C Guballa ◽  
M Hirschner ◽  
A Binder ◽  
...  

2021 ◽  
pp. 105332
Author(s):  
Joachim Brumberg ◽  
Anastasia Kuzkina ◽  
Constantin Lapa ◽  
Sona Mammadova ◽  
Andreas Buck ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Benedict Tanudjojo ◽  
Samiha S. Shaikh ◽  
Alexis Fenyi ◽  
Luc Bousset ◽  
Devika Agarwal ◽  
...  

Abstractα-Synuclein is critical in the pathogenesis of Parkinson’s disease and related disorders, yet it remains unclear how its aggregation causes degeneration of human dopaminergic neurons. In this study, we induced α-synuclein aggregation in human iPSC-derived dopaminergic neurons using fibrils generated de novo or amplified in the presence of brain homogenates from Parkinson’s disease or multiple system atrophy. Increased α-synuclein monomer levels promote seeded aggregation in a dose and time-dependent manner, which is associated with a further increase in α-synuclein gene expression. Progressive neuronal death is observed with brain-amplified fibrils and reversed by reduction of intraneuronal α-synuclein abundance. We identified 56 proteins differentially interacting with aggregates triggered by brain-amplified fibrils, including evasion of Parkinson’s disease-associated deglycase DJ-1. Knockout of DJ-1 in iPSC-derived dopaminergic neurons enhance fibril-induced aggregation and neuronal death. Taken together, our results show that the toxicity of α-synuclein strains depends on aggregate burden, which is determined by monomer levels and conformation which dictates differential interactomes. Our study demonstrates how Parkinson’s disease-associated genes influence the phenotypic manifestation of strains in human neurons.


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