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本文引用的文献

1
Meningeal inflammation and cortical demyelination in acute multiple sclerosis.急性多发性硬化症中的脑膜炎症和皮质脱髓鞘。
Ann Neurol. 2018 Dec;84(6):829-842. doi: 10.1002/ana.25365. Epub 2018 Nov 30.
2
Exploring the heterogeneity of MS lesions using positron emission tomography: a reappraisal of their contribution to disability.利用正电子发射断层扫描技术探索多发性硬化症病灶的异质性:对其导致残疾的作用的再评估。
Brain Pathol. 2018 Sep;28(5):723-734. doi: 10.1111/bpa.12641.
3
Integrated magnetic resonance imaging and [ C]-PBR28 positron emission tomographic imaging in amyotrophic lateral sclerosis.肌萎缩侧索硬化症的磁共振成像与[ C]-PBR28 正电子发射断层扫描成像的整合。
Ann Neurol. 2018 Jun;83(6):1186-1197. doi: 10.1002/ana.25251.
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Distinct dynamic profiles of microglial activation are associated with progression of Alzheimer's disease.小胶质细胞激活的不同动态特征与阿尔茨海默病的进展相关。
Brain. 2018 Jun 1;141(6):1855-1870. doi: 10.1093/brain/awy079.
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Inflammatory intrathecal profiles and cortical damage in multiple sclerosis.多发性硬化症中的炎症性鞘内特征和皮质损伤。
Ann Neurol. 2018 Apr;83(4):739-755. doi: 10.1002/ana.25197.
6
Loss of 'homeostatic' microglia and patterns of their activation in active multiple sclerosis.“稳态”小胶质细胞的丧失及其在活动性多发性硬化症中的激活模式。
Brain. 2017 Jul 1;140(7):1900-1913. doi: 10.1093/brain/awx113.
7
Reply.回复。
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8
Slow expansion of multiple sclerosis iron rim lesions: pathology and 7 T magnetic resonance imaging.多发性硬化症铁环病变的缓慢扩展:病理学与7T磁共振成像
Acta Neuropathol. 2017 Jan;133(1):25-42. doi: 10.1007/s00401-016-1636-z. Epub 2016 Oct 27.
9
Neuroinflammatory component of gray matter pathology in multiple sclerosis.多发性硬化症中灰质病理的神经炎症成分
Ann Neurol. 2016 Nov;80(5):776-790. doi: 10.1002/ana.24791. Epub 2016 Oct 25.
10
Slowly eroding lesions in multiple sclerosis.多发性硬化症中的缓慢侵蚀性病变
Mult Scler. 2017 Mar;23(3):464-472. doi: 10.1177/1352458516655403. Epub 2016 Jul 11.

多模态 7 特斯拉 MRI 和 C-PBR28 PET 对多发性硬化皮质炎症特征的研究

Profiles of cortical inflammation in multiple sclerosis by C-PBR28 MR-PET and 7 Tesla imaging.

机构信息

Department of Radiology, Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA/ Harvard Medical School, Boston, MA, USA.

Department of Radiology, Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA.

出版信息

Mult Scler. 2020 Oct;26(12):1497-1509. doi: 10.1177/1352458519867320. Epub 2019 Aug 1.

DOI:10.1177/1352458519867320
PMID:31368404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6994367/
Abstract

BACKGROUND

Neuroinflammation with microglia activation is thought to be closely related to cortical multiple sclerosis (MS) lesion pathogenesis.

OBJECTIVE

Using C-PBR28 and 7 Tesla (7T) imaging, we assessed in 9 relapsing-remitting multiple sclerosis (RRMS) and 10 secondary progressive multiple sclerosis (SPMS) patients the following: (1) microglia activation in lesioned and normal-appearing cortex, (2) cortical lesion inflammatory profiles, and (3) the relationship between neuroinflammation and cortical integrity.

METHODS

Mean C-PBR28 uptake was measured in focal cortical lesions, cortical areas with 7T quantitative T* (q-T*) abnormalities, and normal-appearing cortex. The relative difference in cortical C-PBR28 uptake between patients and 14 controls was used to classify cortical lesions as either active or inactive. Disease burden was investigated according to cortical lesion inflammatory profiles. The relation between q-T* and C-PBR28 uptake along the cortex was assessed.

RESULTS

C-PBR28 uptake was abnormally high in cortical lesions in RRMS and SPMS; in SPMS, tracer uptake was significantly increased also in normal-appearing cortex. C-PBR28 uptake and q-T* correlated positively in many cortical areas, negatively in some regions. Patients with high cortical lesion inflammation had worse clinical outcome and higher intracortical lesion burden than patients with low inflammation.

CONCLUSION

C-PBR28 and 7T imaging reveal distinct profiles of cortical inflammation in MS, which are related to disease burden.

摘要

背景

神经炎症伴小胶质细胞激活被认为与皮质多发性硬化(MS)病变发病机制密切相关。

目的

使用 C-PBR28 和 7 特斯拉(7T)成像,我们评估了 9 例复发缓解型多发性硬化症(RRMS)和 10 例继发进展型多发性硬化症(SPMS)患者:(1)病变和正常皮质的小胶质细胞激活,(2)皮质病变炎症特征,以及(3)神经炎症与皮质完整性之间的关系。

方法

在局灶性皮质病变、7T 定量 T*(q-T*)异常的皮质区域和正常皮质中测量 C-PBR28 的平均摄取量。用患者与 14 名对照者皮质 C-PBR28 摄取量的相对差异,将皮质病变分类为活跃或不活跃。根据皮质病变炎症特征研究疾病负担。评估 q-T*和 C-PBR28 沿皮质摄取量之间的关系。

结果

RRMS 和 SPMS 患者的皮质病变中 C-PBR28 摄取异常升高;SPMS 患者正常皮质中示踪剂摄取也显著增加。C-PBR28 摄取量和 q-T*在许多皮质区域呈正相关,在一些区域呈负相关。皮质病变炎症程度高的患者比炎症程度低的患者临床预后差,皮质内病变负担高。

结论

C-PBR28 和 7T 成像揭示了 MS 皮质炎症的不同特征,与疾病负担有关。

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