Figure 2 Interactome analyses in bvFTD

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Figure Pedigrees of the SCA42 families identified in this study
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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 Genomic and facial overview of the microduplications overlapping the GRIN2D gene found in the retrieved patients Genomic and facial overview of.
Figure 3 Pedigree of familial idiopathic transverse myelitis
Figure 1 Box plot of the venous diameter in lesions
Figure 2 Needle biopsy of the left vastus lateralis
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 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.
Figure 1 Comparison of miR-150-5p (log scale), prednisone dose (mg), and QMG score between the thymectomy (ETTX) and prednisone groups Comparison of miR-150-5p.
Figure Pedigree of the family
Figure 1 Linear relationship between CSF inflammation and glucose in meningitis; analysis stratified by diagnostic category (aseptic, n = 115 and microbial,
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 Association of hippocampal subfield volumes to cognition by neopterin level, volumes, and cognition adjusted for age, education, race, sex, and.
Figure 1 Dominant and recessive missense and nonsense variants in neurofilament light (NEFL)‏ Dominant and recessive missense and nonsense variants in.
Figure WDR45 sequence changes in patients A and B
Figure 1 ROC curve of ASFMR1-TV2
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 5 Neurite structure is not disrupted by the lack of neurofilament light (NEFL)‏ Neurite structure is not disrupted by the lack of neurofilament.
Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.
Figure 3 Transport activity of human SLC25A4 and SLC25A4 p.Lys33Gln
Figure 3 Receiver operating characteristics for CSF glucose (n = 225) and serum/CSF glucose ratio (n = 156) as predictors for microbial meningitis Receiver.
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 3 Mutation carrier–derived lymphoblastoid cell lines (LCLs) show decreased aconitase 2 activity and mitochondrial respiration deficiency compared.
Figure Family tree with the HLA haplotyping of 6 members of the family
Figure 4 Relative abundances of the order Clostridiales and its family members are differentially changed by therapy Relative abundances of the order Clostridiales.
Figure 1 Family pedigree and MRI
Figure Genomic and facial overview of the microduplications overlapping the GRIN2D gene found in the retrieved patients Genomic and facial overview of.
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 Diagrammatic levodopa pharmacokinetics after single doses of immediate release (IR) carbidopa/levodopa (CD/LD) and 3 strengths of extended release.
Figure 1 [18F]florbetapir standardized uptake value ratio analytical method [18F]florbetapir standardized uptake value ratio analytical method Flowchart.
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 Responder rates of patients at 4 weeks compared with prevaccinated levels Responder rates of patients at 4 weeks compared with prevaccinated levels.
Figure 6 Cellular composition after tissue dissociation
Figure 1 Histamine flare in patients and controls
Figure 3 Similar but restricted distributions of pathogenic variants in the P domain Similar but restricted distributions of pathogenic variants in the.
Figure 2 Changes in fatigue under treatment
Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.
Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.
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 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 4 CHCHD2 but not TOP1MT expression rescues molecular defects
Figure 1 bvFTD PINBPA network
Figure 1 Schematic representation of FOXG1 gene, protein domain structure, and positions of FOXG1 mutations Schematic representation of FOXG1 gene, protein.
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 2 LMNB1 mRNA expression
Figure 1 ASO functions ASO functions Target mRNA fates depending on ASO mechanism of action that is determined by where the ASO is targeted and by ASO.
Figure 3 Within-group comparisons (before–after)‏
Figure 2 Between-group comparisons
Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.
Figure 2 Time from incident ADS event to MS diagnosis
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.
Figure 4 Western blotting
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Figure 2 Interactome analyses in bvFTD Interactome analyses in bvFTD (A) Protein network built through the W-PPI-NA pipeline around the 63 genes prioritized by the PINBPA protocol. The seeds are depicted in pink and their interactors in blue. (B) Inter-interactome degree distribution curve reporting the number of nodes (x-axis) able to bridge an N number of seeds (y-axis). The IIHs are the nodes marked by the rectangle. (C) List of IIHs reporting the number of seeds that they bridge and associated %. *UBC has been reported yet ignored as it is likely a false positive (as it may indicate unspecific binding of ubiquitin to proteins tagged for degradation). (D) Core of the network around the IIHs, which are depicted in pink. Luke W. Bonham et al. Neurol Genet 2018;4:e266 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.