Figure 4 Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Prevention of onset of.

Slides:

Advertisements

Similar presentations

Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)

Advertisements

Figure 1 Box plot of the venous diameter in lesions

Cognitive deficits in APPPS1‐21 mice.

Figure 2. Change in total PSPRS score from baseline to each study visit for all participants Change in total PSPRS score from baseline to each study visit.

Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.

Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.

Figure 3 JCV index changes in JCV+ patients

Figure Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.

Figure 3 Age, pretreatment, sex, and leukopenia do not influence CD19+ cell repopulation Age, pretreatment, sex, and leukopenia do not influence CD19+

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.

Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

Figure 2 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.

Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

Figure 3 Gene expression in CSF cell pellets

Figure 6 Laquinimod treatment of spontaneous EAE prevents progression and reduces the frequency of Tfh cells Laquinimod treatment of spontaneous EAE prevents.

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 2 Mean serum concentrations of BIIB033 vs time(A) Single ascending dose study and (B) multiple ascending dose study. Mean serum concentrations of.

Figure 1 Peripheral blood leukocyte subset counts during dimethyl fumarate treatmentComplete blood cell counts were obtained at baseline (n = 34) and at.

Dominic M. Walsh, Dennis J. Selkoe Neuron

Figure 2 DTI values between the hepatitis C group and controls(A) DTI FA values, (B) DTI diffusion values. *Statistically significant at FDR-adjusted p.

Age‐related amyloid deposition in APPPS1‐21 mice.

Figure 1 GABAB expression in the thymus(A–C) Staining of thymus tissue with anti-cytokeratin (A) and anti-GABAB antibody (B, C double immunofluorescence).

Figure 2 JCV index JCV index (A) Fifty samples of natalizumab-treated patients with multiple sclerosis were assessed twice for their anti-JCV antibody.

Figure 1 Schematic overview of flow cytometry Schematic overview on the analysis of peripheral immune cells by flow cytometry. Schematic overview of flow.

Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.

Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

Figure 1 JCV serostatus JCV serostatus (A) Serostatus of 1,921 natalizumab-treated patients with multiple sclerosis, with JCV− patients shown in black.

Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.

Figure 4 Laquinimod treatment suppresses development of spontaneous EAE Laquinimod treatment suppresses development of spontaneous EAE (A) 2D2 × Th mice.

Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.

Lauren Brash et al. BTS 2018;3:

Figure 5 ADP-induced inflammatory responses require P2Y12 receptors in human microgliaIncreasing concentrations of ADP (5, 50, and 200 μM) increased tumor.

Figure 2 P2Y12 expression is upregulated in M2-polarized human microglia(A, B) Using TaqMan quantitative real-time PCR, P2Y12 expression was measured in.

Figure 1 Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo.

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 2 Peripheral blood lymphocyte subset counts during dimethyl fumarate treatment(A) Lymphocyte subsets were obtained at baseline (n = 21) and at month.

Figure Leptomeningeal inflammationPostcontrast T1-weighted MRI: abnormal leptomeningeal enhancement over the frontoparietal lobes and interhemispheric.

Figure 2 Induced deletion of CXCR2 on oligodendrocyte lineage cells after tamoxifen injection in Cxcr2-cKO mice Induced deletion of CXCR2 on oligodendrocyte.

Figure 1 Examination of MuSK antibody levels and B-cell subsetsFlow cytometric analysis (n = 13) using standardized Human Immunology Project Consortium.

Figure 3 Laquinimod (LAQ) reduces microglia infiltration and acute axonal damage after 6 weeks of cuprizone Laquinimod (LAQ) reduces microglia infiltration.

Figure 2 CD4+ T-cell subsets fluorescence-activated cell sorting analysis in peripheral blood mononuclear cells of patients with multiple sclerosis treated.

Figure 2 Changes in fatigue under treatment

Figure 2 Assessment of systemic disease activityTc99 scintigraphy (A) and fluorodeoxyglucose PET imaging (B, C) at disease onset 2 years before acute deterioration.

Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.

Figure 3 Effect of IVIg on endogenous relative concentration (in mAb equivalents) of JCV AbSix patients shown in this figure have had John Cunningham virus.

Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.

Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.

Figure 3 Mice with antibodies to NMDARs have decreased hippocampal total protein levels of NMDARs Mice with antibodies to NMDARs have decreased hippocampal.

Biphasic ambulatory activity and reduced avoidance in Id2−/− mice.

Figure 3 Downregulation of T-bet expression in brain-infiltrating MIF−/− CD4+ T cells Macrophage migration inhibitory factor (MIF)−/− and wild-type (Wt)

Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.

Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504

Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.

Figure 2 Cell-based assay demonstrating differential binding of AChR antibodies to the adult and fetal receptorsThe fetal (gamma subunit specific) and.

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

Figure 1 EAE severity and CNS pathology in Dex-treated MIF−/− and Wt mice Wild-type (Wt) and macrophage migration inhibitory factor (MIF)−/− mice were.

Figure 2 Effect of Dex on cytokine production by MIF−/− or Wt T cells in EAE Wild-type (Wt) and macrophage migration inhibitory factor (MIF)−/− mice were.

Figure 2 Between-group comparisons

Both the MMP9 and MMP2 systems are activated by anti-Aβ antibodies, IVIg, and mouse IgG. Both the MMP9 and MMP2 systems are activated by anti-Aβ antibodies,

Figure 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.

Pioglitazone induces the clearance of amyloid in APP/PS1 mice.

Impact of eNOS expression and treatment with GSNO on prostate tumor growth. Impact of eNOS expression and treatment with GSNO on prostate tumor growth.

Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.

Figure 1 Glutamine antagonist JHU083 inhibits T-cell proliferation in vitro Glutamine antagonist JHU083 inhibits T-cell proliferation in vitro T-cell proliferation.

Presentation transcript:

Figure 4 Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Five-month-old female Dutch APP E693Q transgenic mice were given weekly subcutaneous injections of either saline (n = 11) or 2 g/kg neat Baxter IG (n = 12), 2 g/kg IG depleted of anti-fibril Aβ antibodies (fibril Aβ-affinity-depleted IG; n = 11), 2 g/kg IG depleted of anti-oligomer Aβ antibodies (oligomer Aβ-affinity-depleted IG; n = 11), or 2 g/kg IG depleted of both anti-oligomer and anti-fibril Aβ antibodies (Aβ-affinity-depleted IG; n = 11) for 3 months. Unlike treatment of saline, fibril Aβ-affinity-depleted IG and Aβ-affinity-depleted IG, treatment of IG prevented onset of behavioral deficits in novel object recognition (A), Y-maze spontaneous alternation (B), and contextual/cued fear conditioning (C) without affecting anxiety-like behavior in the elevated plus maze (C) in Dutch APP E693Q transgenic mice. Treatment of oligomer Aβ-affinity-depleted IG prevented onset of behavioral deficit in novel object recognition (A) in Dutch APP E693Q transgenic mice. *p < 0.05; **p < 0.01; 1-way analysis of variance with Bonferroni post hoc analyses. Data expressed as mean ± SEM. Aβ = β-amyloid; IG = Immune Globulin. Elysse M. Knight et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e237 © 2016 American Academy of Neurology