28 research outputs found

    Additional file 6: of Poly-GR dipeptide repeat polymers correlate with neurodegeneration and Clinicopathological subtypes in C9ORF72-related brain disease

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    Table S2. Correlation between DPR and aDMA inclusions. P-values are from Pearson’s test of correlation. Significant p-values (< 0.05) are indicated in bold. FCtx frontal cortex, DF dentate fascia, CA - cornu ammonis, MCtx motor cortex. (DOCX 14 kb

    Additional file 4: of Poly-GR dipeptide repeat polymers correlate with neurodegeneration and Clinicopathological subtypes in C9ORF72-related brain disease

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    Figure S3. Dot plot graph of semiquantitative assessment of neurodegeneration and DPR. Note that X axis is neurodegeneration score (0 to 3), Y-axis is density of DPR. FCtx - frontal cortex, DF - dentate fascia, CA4 - cornu ammonis sector 4. (TIF 1325 kb

    Additional file 7: of Poly-GR dipeptide repeat polymers correlate with neurodegeneration and Clinicopathological subtypes in C9ORF72-related brain disease

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    Figure S5 Comparison of immunostaining with aDMA between C9ORF72 cases and non- neurodegeneration control in parahippocampal cortex. The nuclear signal of aDMA is variable in both cases and controls. Note sparse cytoplasmic inclusions labeled with aDMA in in C9ORF72 cases (arrows). Scale bar represents 50 ΟM. (TIF 2898 kb

    Additional file 3: of Poly-GR dipeptide repeat polymers correlate with neurodegeneration and Clinicopathological subtypes in C9ORF72-related brain disease

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    Table S1. Quantitative assessment of DPR density by color deconvolution algorithm in clinicopathologic subgroups of C9ORF72-related disease. In frontal cortex, p = 0.019, FTLD vs. FTLD-MND. In CA4, p = 0.055, FTLD vs. FTLD-MND. In CA2/3, p = 0.03, FTLD vs. FTLD-MND. Significant p-values (< 0.05) are indicated in bold. All variables were analyzed with Kruskal-Wallis ANOVA on Ranks and data are displayed as median (25th and 75th range). *Statistically significant p-value (p < 0.05); all p-value for ANOVA on Ranks comparison of all three groups. FCtx = frontal cortex, MCtx = Motor cortex, DF dentate fascia, CA hippocampal subfields. (DOCX 15 kb

    Additional file 2: of Poly-GR dipeptide repeat polymers correlate with neurodegeneration and Clinicopathological subtypes in C9ORF72-related brain disease

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    Figure S2. Correlation between manual counts and positive pixel burden from color deconvolution in poly-GR staining. Plot shows the correlation of manual counts of neuronal cytoplasmic inclusions and positive pixel burden from color deconvolution in poly-GR staining. The line shows linear regression CD color deconvolution. Ctx frontal cortex, DF dentate fascia, CA - cornu ammonis, MCtx motor cortex. (TIF 2581 kb

    Additional file 5: of Poly-GR dipeptide repeat polymers correlate with neurodegeneration and Clinicopathological subtypes in C9ORF72-related brain disease

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    Figure S4. Western blot analysis of aDMA and sDMA in brains of C9FLTD-MND and sporadic FTLD-MND. The high molecular weight aDMA and sDMA signals are visible in c9FTD/ALS, but not in sporadic FTD/ALS cases. (TIF 2960 kb

    Additional file 2: Figure S2. of Neonatal AAV delivery of alpha-synuclein induces pathology in the adult mouse brain

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    Neither ThioS positive structures nor neurodegeneration are observed in AAV-αsyn animals. (a-i) Sagittal brain sections were incubated with anti human asyn antibody followed by 5 min in 1% thioS solution. Thalamus (a-c) and cortex (d-f) of AAV-asyn animal show strong asyn immunoreactivity (a, d) that is not thioS- positive (b, e). As a control, human DLBD brain was co-stained in parallel. Cortical Lewy bodies positive for human asyn (g) are reactive to thioS (h, i). Representative images of NeuN-labeled cells in the cortex of AAV-asyn (n = 9) and AAV-venus (n = 7) at 6 months of age (k). Quantification of NeuN-positive cells in the whole cortex (area delineated in blue). Data are presented as as mean ± S.E.M means. Scale bars in i = 40 μm and applied to a-h; Scale bars in k = 2 mm. Abbreviation: DLBD; Diffuse Lewy Body Disease. (PDF 1541 kb

    Additional file 1: Figure S1. of Neonatal AAV delivery of alpha-synuclein induces pathology in the adult mouse brain

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    Representative intensity of Human αsyn immunostaining (a) Photomicrographs representative of the variability of expression observed in the different group of animals at 1, 3 and 6 months of age (b) Level of expression of the transgene was assessed by western blot in AAV-αsyn at 3 months of age and compared to transgenic mice overexpressing αsyn under Thy1 promoter (line 61) at the same age. Antibody recognizing human and mouse αsyn was used (clone 42). (c) Quantification of the western blot shows αsyn level increase of 2.93 ± 0.33 fold in the AAV-αsyn animals and 3.23 ± 0.12 fold in the line 61. .The data are expressed as the amount of total level of αsyn normalized to actin (*, p < 0.05) and are from 3 repeated experiments. (PDF 1678 kb

    Additional file 1: of TMEM106B haplotypes have distinct gene expression patterns in aged brain

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    Table S1. Tissue samples available and selected for inclusion in this study. Table S2. DEGS in TCX. Positive fold change represents higher gene expression in SS than TT. Negative fold change represents lower gene expression in SS than TT. Table S3. DEGS in CER. Positive fold change represents higher gene expression in SS than TT. Negative fold change represents lower gene expression in SS than TT. Table S4. Overlapping genes between TCX and CER based on top 500 genes with |FC| ≥ 1.2 ranked by unadjusted p value. Table S5. Enrichment of modules for their respective DEG signatures. Table S6. Significant modules identified in the TCX and CER matched cases. Table S7. Significant modules identified in separate disease groups in TCX and CER. Table S8. Significant modules identified in the TCX and CER controls. (DOCX 54 kb
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