Figure 1 Biomarkers associated with different clinical phases in MS

Slides:



Advertisements
Similar presentations
© 2014 Direct One Communications, Inc. All rights reserved. 1 A New Era of Therapy in Multiple Sclerosis: Balancing the Options and Challenges Ahead Jennifer.
Advertisements

Potassium Channel KIR4.1 as an Immune Target in Multiple Sclerosis.
Date of download: 6/30/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Quantification and Functional Characterization of.
Harry Irving, Hung Jiew Lee, John Parratt
Four Known Types of MS Clinically isolated syndrome (CIS)
Nat. Rev. Neurol. doi:10/1038/nrneurol
Copyright © 2011 American Medical Association. All rights reserved.
Nat. Rev. Neurol. doi: /nrneurol
Copyright © 2010 American Medical Association. All rights reserved.
Figure 1 Perivenous distribution of multiple sclerosis lesions
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Volume 18, Issue 1, Pages (February 2011)
Figure 2 The US Centers for Disease Control and
Figure 4 Time course of the development of physiological changes
Nat. Rev. Neurol. doi: /nrneurol
Figure 4 Cerebrospinal fluid levels of neurofilament light chain
Figure Model contrasting the potential role of antibodies to myelin oligodendrocyte glycoprotein (MOG) or aquaporin-4 (AQP4) in opticospinal inflammationMOG-specific.
Nat. Rev. Neurol. doi: /nrneurol
Figure 7 Clinical options for HCC therapy
Nat. Rev. Neurol. doi: /nrneurol
Nat. Rev. Neurol. doi: /nrneurol
Assessing Disease Progression in MS Treatment
Figure 3 Proportion of patients for whom NEDA
Figure 4 Neuromyelitis optica spectrum disorder brain lesions
Nat. Rev. Neurol. doi: /nrneurol
Nat. Rev. Neurol. doi: /nrneurol
Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.
Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.
Figure 3 Archetypal MS clinical course depicted over 20 years
Figure 1 Associations between baseline cerebrospinal fluid
Figure 1 Percent positivity by clinical feature Overall, 6
Figure 3 LGI1 and Caspr2 immunohistochemistry on rat brain
Figure 1 Gliomas—genetic landscape and biomarkers
Nat. Rev. Neurol. doi: /nrneurol
Nat. Rev. Neurol. doi: /nrneurol
Figure 1 Clinical correlates of neurodegeneration in MS
Figure 3 Genetic pleiotropy in ALS
Figure 1 Evolution of multiple sclerosis
Nat. Rev. Neurol. doi: /nrneurol
Figure 2 Primary and secondary outcomes reported in multiple sclerosis (MS) disease-modifying therapy (DMT) clinical trials Primary and secondary outcomes.
Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.
Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.
Nat. Rev. Neurol. doi: /nrneurol
Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.
Figure 3 Potential interplay between physiological
Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)
Figure 2. ROC curves for different group comparisons
Figure 4 Neuropathology of MOG and AQP4 antibody–associated demyelinating lesions in the brain The biopsy specimen revealed a small actively demyelinating.
Nat. Rev. Mater. doi: /natrevmats
Nat. Rev. Neurol. doi: /nrneurol
Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,
Nat. Rev. Neurol. doi: /nrneurol
H&E, 100x
Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.
Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.
Figure 7 VEGF as a mediator of neuroinflammatory disease
Figure 1. Antibodies to MOG in a proportion of adult patients with MS
Figure Correlation between the Kurtzke Expanded Disability Status Scale and the relative expression of hsa-miR-337-3p Correlation between the Kurtzke Expanded.
Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)
Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.
Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.
Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing.
Figure 1 Levels of miR-150 are elevated in patients with multiple sclerosis (MS) and patients with clinically isolated syndrome (CIS) who convert to MS.
Nat. Rev. Neurol. doi: /nrneurol
Figure 2. Detection of KIR4.1 autoantibodies using LIPS
Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.
Figure 3 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.
This program will include a discussion of data that were presented in abstract form. These data should be considered preliminary until published in a.
Figure 2 Antibodies to MOG detected with anti-human IgG (H + L) as the secondary antibody(A) Schematic of the human MOG proteins tested. Antibodies to.
Figure 4 C5B3 decreased NMOSD mouse model lesions in vivo
Presentation transcript:

Figure 1 Biomarkers associated with different clinical phases in MS Figure 1 | Biomarkers associated with different clinical phases in MS. This overview shows how biomarkers discussed in this Review are linked to specific clinical stages of MS. The arrows indicate expression changes in MS. ± indicates that the antibody can be either present or absent. Abbreviations: κFLC, κ free light chain; AQP4, aquaporin 4; CHI3L1, chitinase-3-like protein 1; CIS, clinically isolated syndrome; CSF, cerebrospinal fluid; CXCL13, C–X–C motif chemokine 13; DMT, disease-modifying therapy; GFAP, glial fibrillary acidic protein; KIR4.1, potassium channel, inwardly rectifying subfamily J member 10; miR, microRNA; MOG-IgG, IgG against myelin oligodendrocyte glycoprotein; MS, multiple sclerosis; MRZ, measles–rubella–varicella zoster; NAA, N-acetylaspartate; NAbs, neutralizing antibodies (against IFN-β or natalizumab); NfL/H, neurofilament light/heavy chain; NMO, neuromyelitis optica; OCBs, oligoclonal bands; PPMS, primary progressive MS; RRMS, relapsing–remitting MS; SPMS, secondary progressive MS. Teunissen, C. E. et al. (2015) Body fluid biomarkers for multiple sclerosis—the long road to clinical application Nat. Rev. Neurol. doi:10.1038/nrneurol.2015.173