Imaging central nervous system myelin by positron emission tomography in multiple sclerosis using [methyl‐<sup>11</sup>C]‐2‐(4′‐methylaminophenyl)‐ 6‐hydroxybenzothiazole

Stankoff, Bruno; Freeman, Léorah; Aigrot, Marie‐Stéphane; Chardain, Audrey; Dollé, Frédéric; Williams, Anna; Galanaud, Damien; Armand, Lucie; Lehericy, Stéphane; Lubetzki, Catherine; Zalc, Bernard; Bottlaender, Michel

doi:10.1002/ana.22320

Cited by 188 publications

(182 citation statements)

References 35 publications

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“…patients cannot be achieved without significant advances in imaging techniques (such as magnetic transfer ratio and diffuse tensor imaging) that measure myelin content and tissue organization using conventional magnetic resonance imagers [80][81][82][83] . As these techniques become more standardized and gain wider use, they will greatly enhance our ability to read the progression of the myelination process in patients.…”

Section: The Demonstration Of Successful Remyelination In Msmentioning

confidence: 99%

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Zhang

Guo

2013

Neurosci. Bull.

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Multiple sclerosis (MS) is a chronic and devastating autoimmune demyelinating disease of the central nervous system. With the increased understanding of the pathophysiology of this disease in the past two decades, many disease-modifying therapies that primarily target adaptive immunity have been shown to prevent exacerbations and new lesions in patients with relapsing-remitting MS. However, these therapies only have limited efficacy on the progression of disability. Increasing evidence has pointed to innate immunity, axonal damage and neuronal loss as important contributors to disease progression. Remyelination of denuded axons is considered an effective way to protect neurons from damage and to restore neuronal function. The identification of several key molecules and pathways controlling the differentiation of oligodendrocyte progenitor cells and myelination has yielded clues for the development of drug candidates that directly target remyelination and neuroprotection. The long-term efficacy of this strategy remains to be evaluated in clinical trials. Here, we provide an overview of current and emerging therapeutic concepts, with a focus on the opportunities and challenges for the remyelination approach to the treatment of MS.

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Section: The Demonstration Of Successful Remyelination In Msmentioning

confidence: 99%

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Zhang

Guo

2013

Neurosci. Bull.

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“…A noninvasive imaging technique such as PET could differentiate and quantify MS hallmarks and thus could be an important tool to monitor therapeutic response and help to better understand drug mechanisms. The potential of PET for imaging several hallmarks of MS was shown in animal models (4)(5)(6)(7)(8)(9)(10)(11)(12)(13) and in patients (14)(15)(16)(17)(18)(19)(20)(21)(22), but different hallmarks were not longitudinally measured at the same time in these studies. Despite the fact that MS comprises multiple aspects that are important for therapy monitoring and drug development, PET is not yet regularly applied in a clinical setting.…”

mentioning

confidence: 91%

PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model

et al. 2014

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“…The proposed binding has low affinity and is likely not saturable because of the large amount of myelin in the brain. In other words, a high concentration of unlabeled ligand would be required to saturate the binding of amyloid radioligands to cerebral white matter (24). Moreover, it has been estimated that ROIs defined for the cerebral cortex contain about 60% of gray matter and 30% of white matter (25).…”

Section: Discussionmentioning

confidence: 99%

Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer ¹¹C-AZD2184

Ito¹,

Shimada²,

Shinotoh³

et al. 2014

J Nucl Med

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Characteristic neuropathologic changes in Alzheimer disease (AD) are amyloid-β deposits and neurofibrillary tangles. Recently, a new radioligand for amyloid senile plaques, 11 C-labeled 5-(6-{[tertbutyl(dimethyl)silyl]oxy}-1,3-benzothiazol-2-yl)pyridin-2-amine ( 11 C-AZD2184), was developed, and it was reported to show rapid brain uptake followed by rapid washout. In this study, 11 C-AZD2184 binding in control subjects and AD patients was examined in more detail by compartment model analysis using a metabolite-corrected arterial input function. The accuracy of simplified quantitative methods using a reference brain region was also evaluated. Methods: After intravenous bolus injection of 11 C-AZD2184, a dynamic PET scan was obtained for 90 min in 6 control subjects and 8 AD patients. To obtain the arterial input function, arterial blood sampling and high-performance liquid chromatography analysis were performed. Results: Time-activity curves in all brain regions could be described using the standard 2-tissue-compartment model. The total distribution volume ratios to reference region (DVR) in cerebral cortical regions were significantly higher in AD patients than in control subjects. Although there was no conspicuous accumulation of radioactivity in white matter as compared with other amyloid radioligands, DVR values in the centrum semiovale were more than 1 for both control subjects and AD patients, suggesting binding to myelin. The standardized uptake value ratio calculated from integrated time-activity curves in brain regions and the reference region was statistically in good agreement with DVR. Conclusion: Although the white matter binding of 11 C-AZD2184 may have some effect on cortical measurement, it can be concluded that the kinetic behavior of 11 C-AZD2184 is suitable for quantitative analysis. The standardized uptake value ratio can be used as a validated measure of 11 C-AZD2184 binding in clinical examinations without arterial input function.

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Imaging central nervous system myelin by positron emission tomography in multiple sclerosis using [methyl‐¹¹C]‐2‐(4′‐methylaminophenyl)‐ 6‐hydroxybenzothiazole

Abstract: PIB could be used as an imaging marker to quantify myelin loss and repair in demyelinating diseases.

Cited by 188 publications

References 35 publications

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model

Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer ¹¹C-AZD2184

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Imaging central nervous system myelin by positron emission tomography in multiple sclerosis using [methyl‐11C]‐2‐(4′‐methylaminophenyl)‐ 6‐hydroxybenzothiazole

Abstract: PIB could be used as an imaging marker to quantify myelin loss and repair in demyelinating diseases.

Cited by 188 publications

References 35 publications

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

PET Imaging of Disease Progression and Treatment Effects in the Experimental Autoimmune Encephalomyelitis Rat Model

Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer 11C-AZD2184

Contact Info

Product

Resources

About

Imaging central nervous system myelin by positron emission tomography in multiple sclerosis using [methyl‐¹¹C]‐2‐(4′‐methylaminophenyl)‐ 6‐hydroxybenzothiazole

Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer ¹¹C-AZD2184