Quantitative magnetic resonance imaging towards clinical application in multiple sclerosis

Granziera, Cristina; Wuerfel, Jens; Barkhof, Frederik; Calabrese, Massimiliano; Stefano, Nicola De; Enzinger, Christian; Evangelou, Nikos; Filippi, Massimo; Geurts, Jeroen J. G.; Reich, Daniel S.; Rocca, Maria; Ropele, Stefan; Rovira, Àlex; Sati, Pascal; Toosy, Ahmed; Vrenken, Hugo; Wheeler-Kingshott, C; Kappos, Ludwig

doi:10.1093/brain/awab029

Cited by 105 publications

(109 citation statements)

References 195 publications

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“…MRI g-ratios are derived by combining AVF measures from neurite orientation dispersion and density imaging and MVF from MTsat to provide an estimate of myelin thickness. A number of previous studies have identified an association between T 1 and magnetization transfer ratio values, 18 and myelin loss, including paired MRI–neuropathology studies. 18 , 19 Our analysis, however, found significant correlation between lesional g-ratio and elevated serum neurofilament, whereas MT and T 1 measures alone showed no such association with serum neurofilament.…”

Section: Discussionmentioning

confidence: 99%

“…A number of previous studies have identified an association between T 1 and magnetization transfer ratio values, 18 and myelin loss, including paired MRI–neuropathology studies. 18 , 19 Our analysis, however, found significant correlation between lesional g-ratio and elevated serum neurofilament, whereas MT and T 1 measures alone showed no such association with serum neurofilament. The degree to which g-ratio may provide a more specific surrogate measure of demyelination in early RRMS, and how individual MT and diffusion measures reflect varying proportions of myelin and axonal damage, warrants further evaluation.…”

Section: Discussionmentioning

confidence: 99%

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MRI-derived g-ratio and lesion severity in newly diagnosed multiple sclerosis

York

Martin

Meijboom

et al. 2021

Brain Communications

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Myelin loss is associated with axonal damage in established multiple sclerosis. This relationship is challenging to study in vivo in early disease. Here, we ask whether myelin loss is associated with axonal damage at diagnosis, by combining non-invasive neuroimaging and blood biomarkers. We performed quantitative microstructural MRI and single molecule ELISA plasma neurofilament measurement in 73 patients with newly diagnosed, immunotherapy naïve relapsing-remitting multiple sclerosis. Myelin integrity was evaluated using aggregate g-ratios, derived from magnetization transfer saturation (MTsat) and neurite orientation dispersion and density imaging (NODDI) diffusion data. We found significantly higher g-ratios within cerebral white matter lesions (suggesting myelin loss) compared with normal-appearing white matter (0.61 vs 0.57, difference 0.036, 95% CI 0.029 to 0.043, p < 0.001). Lesion volume (Spearman’s rho rs= 0.38, p < 0.001) and g-ratio (rs= 0.24 p < 0.05) correlated independently with plasma neurofilament. In patients with substantial lesion load (n = 38), those with higher g-ratio (defined as greater than median) were more likely to have abnormally elevated plasma neurofilament than those with normal g-ratio (defined as less than median) (11/23 [48%] versus 2/15 [13%] p < 0.05). These data suggest that, even at multiple sclerosis diagnosis, reduced myelin integrity is associated with axonal damage. MRI-derived g-ratio may provide useful additional information regarding lesion severity, and help to identify individuals with a high degree of axonal damage at disease onset. York, Martin et al. simultaneously measured g-ratio and plasma neurofilament in 73 relapsing-remitting multiple sclerosis patients at diagnosis using advanced MRI and single molecule ELISA. They demonstrate that g-ratio of cerebral white matter lesions varies at diagnosis, and show that high g-ratio of lesions is associated with elevated plasma neurofilament.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MRI-derived g-ratio and lesion severity in newly diagnosed multiple sclerosis

York

Martin

Meijboom

et al. 2021

Brain Communications

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“…Using computational models of biophysical properties of tissues, it is possible to derive metrics sensitive to microstructural integrity and metabolic information of the underlying tissue ( Granziera et al, 2021 ). Ultimately, the aim would be to provide patient-specific metrics able to predict outcomes and contribute to decision making on disease management ( Granziera et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

MAGNIMS recommendations for harmonization of MRI data in MS multicenter studies

Stefano

Battaglini

Pareto

et al. 2022

NeuroImage: Clinical

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“…За даними німецьких дослідників, випадки РС у дітей віком до 10 та 15 років становлять 0,64 та 2,64 на 100 тис. населення відповідно [4].…”

Section: дніпровський медичний інститут традиційної і нетрадиційної медицини дніпро українаunclassified

Efficiency of Experimental Allergic Encephalomyelitis Modeling as an Experimental Model of Multiple Sclerosis

Nefоdov¹,

Miasoied²,

Solomenko³

et al. 2021

Ukr. ž. med. bìol. sportu

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The purpose of the study was the most adequate modeling of multiple sclerosis in the form of autoimmune allergic encephalomyelitis for further use in the study of experimental equivalents of neurodegenerative conditions. Materials and methods. The article highlights the results of the formation of experimental allergic encephalomyelitis, for the induction of which homologous brain homogenates were used, which in terms of encephalitogenicity ranks first among other drugs (homologous, heterogeneous brain and spinal cord homogenates). An encephalitogenic mixture was injected into the connective tissue of the base of the animal's tail at the rate of 0.1 ml per 100 g of body weight. Results and discussion. Experimental allergic encephalomyelitis reproducible by intradermal administration of a homogenate of the brain, spinal cord and peripheral nerves with a Freund's stimulator belongs to a true autoimmune disease of the nervous system and is an experimentally reproducible model of multiple sclerosis. According to the experimental data obtained, the state of the animals showed that the rats of the experimental group lost body weight, had a number of pathological neurological symptoms, which manifested on average from 10-12 days. The increase in symptoms continued for an average of 7 days and was not very stable. Experimental animals had paresis, manifestations of ataxia, walking disorders and urinary and fecal incontinence, lethargy, which corresponded to 1-2 degrees of the rating scale in 13 animals. In 7 rats, paresis of the hind limbs and loss of tail tone were expressed (grade 3). Most of the rats recovered spontaneously within 6-8 days after the onset of clinical manifestations (18-20 days after immunization). According to the requirements of the experiment, during the paralytic stage, the rats had free access to food and water. In addition, our experimental studies on the formation of experimental allergic encephalomyelitis were confirmed morphologically using electron microscopy. Conclusion. The use of this technique for the formation of experimental allergic encephalomyelitis made it possible to obtain a simulated pathological state of multiple sclerosis in the form of experimental allergic encephalomyelitis and can be used in further studies to identify the corresponding patterns, the degree and nature of changes in the immune and nervous systems of the body during the reproduction of an experimental pathological state. The data obtained can serve as a basis for further studies of drugs and their combinations in order to improve and rationalize the pharmacotherapy of multiple sclerosis

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Quantitative magnetic resonance imaging towards clinical application in multiple sclerosis

Cited by 105 publications

References 195 publications

MRI-derived g-ratio and lesion severity in newly diagnosed multiple sclerosis

MRI-derived g-ratio and lesion severity in newly diagnosed multiple sclerosis

MAGNIMS recommendations for harmonization of MRI data in MS multicenter studies

Efficiency of Experimental Allergic Encephalomyelitis Modeling as an Experimental Model of Multiple Sclerosis

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