定量磁化率图
黑质
齿状核
磁共振成像
基底神经节
帕金森病
神经科学
红核
病理
医学
心理学
小脑
中枢神经系统
疾病
核心
放射科
作者
Julio Acosta‐Cabronero,Arturo Cárdenas-Blanco,Matthew J. Betts,Michaela Butryn,José P. Valdés-Herrera,Imke Galazky,Peter J. Nestor
出处
期刊:Brain
[Oxford University Press]
日期:2016-11-11
卷期号:140 (1): 118-131
被引量:150
摘要
Although iron-mediated oxidative stress has been proposed as a potential pathomechanism in Parkinson’s disease, the global distribution of iron accumulation in Parkinson’s disease has not yet been elucidated. This study used a new magnetic resonance imaging contrast, quantitative susceptibility mapping, and state-of-the-art methods to map for the first time the whole-brain landscape of magnetostatic alterations as a surrogate for iron level changes in n = 25 patients with idiopathic Parkinson’s disease versus n = 50 matched controls. In addition to whole-brain analysis, a regional study including sub-segmentation of the substantia nigra into dorsal and ventral regions and qualitative assessment of susceptibility maps in single subjects were also performed. The most remarkable basal ganglia effect was an apparent magnetic susceptibility increase—consistent with iron deposition—in the dorsal substantia nigra, though an effect was also observed in ventral regions. Increased bulk susceptibility, additionally, was detected in rostral pontine areas and in a cortical pattern tightly concordant with known Parkinson’s disease distributions of α-synuclein pathology. In contrast, the normally iron-rich cerebellar dentate nucleus returned a susceptibility reduction suggesting decreased iron content. These results are in agreement with previous post-mortem studies in which iron content was evaluated in specific regions of interest; however, extensive neocortical and cerebellar changes constitute a far more complex pattern of iron dysregulation than was anticipated. Such findings also stand in stark contrast to the lack of statistically significant group change using conventional magnetic resonance imaging methods namely voxel-based morphometry, cortical thickness analysis, subcortical volumetry and tract-based diffusion tensor analysis; confirming the potential of whole-brain quantitative susceptibility mapping as an in vivo biomarker in Parkinson’s disease.
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