Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.

Slides:

Advertisements

Similar presentations

Figure Pedigrees of the SCA42 families identified in this study

Advertisements

Figure 2 ERG amplitude reduction in the follow-up study

Figure 2 Sanger sequencing, conservation, and summary of known ACO2 mutations Sanger sequencing, conservation, and summary of known ACO2 mutations (A)

Figure 1 Summary of prior diagnostic workup in neuromuscular disorder cases Summary of prior diagnostic workup in neuromuscular disorder cases Percentage.

Figure 3 Pedigree of familial idiopathic transverse myelitis

Figure 1 Box plot of the venous diameter in lesions

Figure 1 Regional changes in FA values

Figure 1 Brain MRI findings in the present case

Figure 2 Needle biopsy of the left vastus lateralis

Figure 2 Flow chart of patients who met the inclusion/exclusion criteria for the study Flow chart of patients who met the inclusion/exclusion criteria.

Figure 1 Coronal MRI images showing the evolution of white matter abnormality and atrophy of patient 1 Coronal MRI images showing the evolution of white.

Figure 1 Hierarchical clustering (HCL) outcome of all tested samples with the expression profile of the case report set as unknown Hierarchical clustering.

Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.

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

Figure Pedigree of the family

Figure 1 ERG peak time delay at baseline

Figure 2 Luciferase assays of transiently transfected HEK 293 cells with reporter constructs containing the 766-bp wild-type KCNJ18 or c.-542 T/A mutant.

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

Figure 2 Comparison between noncarriers (−) and carriers (+) of the minor allele of rs (CYP2C19)‏ Comparison between noncarriers (−) and carriers.

Figure 1 Dominant and recessive missense and nonsense variants in neurofilament light (NEFL)‏ Dominant and recessive missense and nonsense variants in.

Figure 3 Temporal trends in FALS incidence

Table 4 Associations in SNP array data between the Braak stage and previously known AD risk loci (341 variants) comparing participants with Braak stage.

Figure 1 All patients with pediatric genetic movement disorders, their genetic diagnoses, and type of genetic investigations All patients with pediatric.

Figure 2 Specific brain MRI findings of 8 patients

Figure 5 Neurite structure is not disrupted by the lack of neurofilament light (NEFL)‏ Neurite structure is not disrupted by the lack of neurofilament.

Figure 1 Characteristics of the German National MS Cohort

Figure 2 Linkage analysis of chromosome 19

Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.

Figure 1 Illustration of white matter– and lesion-associated regions of interest (ROIs)‏ Illustration of white matter– and lesion-associated regions of.

Figure Family tree with the HLA haplotyping of 6 members of the family

Figure 1 Family pedigree and MRI

Figure 3 Analysis of the prognostic value of IL-10–producing B cells or IL-6/IL-10–B-cell ratio measurements in patients with RIS/CIS MS Analysis of the.

Figure 2 Functionally significant genes

Table 2 Rs number, gene, OR, 95% CI, and permutation p value for the statistical significant variants resulted from allelic association analysis association.

Figure 1 Family pedigree and DNA sequencing results

Figure 4 Voltage-clamp recordings of KCNJ18 carrying the patient's SNVs expressed in Xenopus laevis oocytes under control conditions and after application.

Figure 1 [18F]florbetapir standardized uptake value ratio analytical method [18F]florbetapir standardized uptake value ratio analytical method Flowchart.

Figure Alluvial plot of modified Rankin Scale (mRS) scores during and at the end of hospital stay Alluvial plot of modified Rankin Scale (mRS) scores during.

Figure 3 Comparisons of quantitative spinal cord MRI measures and brain atrophy in RIS vs. healthy controls (adjusted for age and sex)‏ Comparisons of.

Figure 3 Voltage-clamp recording of the wild-type KCNJ18 (left) and the KCNJ18 carrying the patient's SNVs (right) expressed in Xenopus laevis oocytes.

Figure 1 Phenotype and functional properties of B cells in MS and HCs at baseline Phenotype and functional properties of B cells in MS and HCs at baseline.

Figure 6 Cellular composition after tissue dissociation

Figure 1 Histamine flare in patients and controls

Figure 1 Considerations for concussed athletes leading to medical care or return to sport (RTS)‏ Considerations for concussed athletes leading to medical.

Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.

Figure 1 Brain MRI Brain MRI (A) Axial fluid-attenuated inversion-recovery images show perilesional edema in both cerebellar hemisphere and hypointense.

Figure 2 Kaplan-Meier survival graphs for 10-year risks of overall and post-90-day recurrent ischemic stroke (IS) and death Kaplan-Meier survival graphs.

Figure 1 Stacked bar chart depicts the proportion of patients with diffusion-weighted imaging (DWI)+ and DWI− scans categorized by index event type TIA.

Figure 1 Annualized percentage brain volume change

Figure 2 BVL according to on-study disability worsening

Figure 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.

Figure 2 Pathogenic deletions upstream of LMNB1

Figure 1 bvFTD PINBPA network

Figure 2 Seizure outcomes

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

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

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

Figure 2 Pedigrees of families and segregation analysis of variants c

Figure Serial brain MRI of the patient with encephalitis and spontaneous recovery accompanying IgLON5 autoimmunity Serial brain MRI of the patient with.

Figure 2 MRIs (cases 2 and 3)‏

Figure 3 Within-group comparisons (before–after)‏

Figure 4 Patient 3 MRI evolution over time

Figure 2 Between-group comparisons

Figure 3 Patient 2 MRI evolution over time before relapse

Figure 2 Time from incident ADS event to MS diagnosis

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 4 Venn diagram for B-cell Sup proteins compared with proteins from exosome-enriched fractions from a human B-cell line Venn diagram for B-cell Sup.

Figure 3 A receiver operating characteristic curve of days to IVMP as a predictor of failure to regain 0.2 logMAR (20/30) vision (AUC 0.84, p < 0.001)‏

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.

Presentation transcript:

Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease The tau-PET signal intensity is overlaid on the patient's own brain MRI rendering using MRIcroGL (nitrc.org/projects/mricrogl). (A) The tau-PET imaging data from the familial prion participant in the bottom row of figure 1 is displayed. (B) The tau-PET imaging data from a patient with young-onset Alzheimer disease is displayed for comparison purposes. David T. Jones et al. Neurol Genet 2018;4:e290 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.