Results: 4

1.
Figure 4

Figure 4. TDP-43 Cytoplasmic Inclusions in Patients with LRRK2 Mutations. From: Clinical and Pathological Characteristics of Patients with Leucine-Rich Repeat Kinase-2 Mutations.

Staining with an antibody to TDP43 revealed the presence of TDP-43 cytoplasmic inclusions in the temporal cortex of patient D (A) and patient E (B, C). Aberrant cytoplasmic TDP-43 inclusions are depicted by arrows, and normal nuclear localization is indicated by arrowheads. Scale bar = 25 μm.

Jason P. Covy, et al. Mov Disord. ;24(1):32-39.
2.
Figure 3

Figure 3. Double-labeling Immunofluorescence Analysis of α-Syn Phosphorylated at Ser129 in Pathological Inclusions of Patients with LRRK2 Mutations. From: Clinical and Pathological Characteristics of Patients with Leucine-Rich Repeat Kinase-2 Mutations.

Double-labeling immunofluorescence analysis demonstrating the presence of α-syn phosphorylated at Ser129 in the vast majority of α-syn inclusions in patients with LRRK2 mutations. Depicted are tissue sections from the SNpc from patient D (A-C) and the amygdala from patient E (D-F). Panels A and D show immunostaining with the rabbit anti-α-syn antibody SNL-4 (green) and panels B and E depicts staining with mouse antiphospho-Ser129 α-syn antibody pSyn 129 (red). The overlays are shown in C and F. Scale bar = 65 μm.

Jason P. Covy, et al. Mov Disord. ;24(1):32-39.
3.
Figure 2

Figure 2. Histological Characterization of Patients with LRRK2 Mutations. From: Clinical and Pathological Characteristics of Patients with Leucine-Rich Repeat Kinase-2 Mutations.

(A, B) Staining for α-syn in the SNpc of patient D demonstrating a dopaminergic neuron with multiple LBs (A) or a typical spheroid (B). (C) Abundant LBs and LNs in the amygdala of patient D. (D) Cortical LBs in the cingulate cortex of patient D. (E) NFTs and tau-positive dystrophic neurites in the hippocampus of patient D. (F) A classical LB in a dopaminergic neurons in SNpc of patient E. (G) Abundant LBs and LNs in hippocampus of patient E. (H, I) NFTs and tau-positive neurites in the hippocampus and entorhinal cortex, respectively, of patient E. Tissue sections were stained with the following antibodies: anti-α-syn antibody Syn 514 (A, C, D, and G), anti-α-syn antibody Syn 211 (B), anti-α-syn antibody LB509 (F), and anti-tau antibody 17026 (E, H and I). Scale bar = 25 μm in A, B, D, E, F, and 50 μm in C, G, H, and I.

Jason P. Covy, et al. Mov Disord. ;24(1):32-39.
4.
Figure 1

Figure 1. Identification of Patients with LRRK2 Mutations and Sequence Alignment of Amino Acid Surrounding the Mutations. From: Clinical and Pathological Characteristics of Patients with Leucine-Rich Repeat Kinase-2 Mutations.

(A) Schematic representation of the LRRK2 protein with major domains. The locations of the R793M, L1165P, and the most common G2109S mutation are indicated. Abbreviations used: LRR, leucine-rich repeat like domain; ROC, Ras of complex; COR, C-terminal of Roc. (B) Portion of sequencing electropherogram showing the region of LRRK2 exon 25 in which the heterozygous c.3494T>C, p.L1165P was identified in Patient E compared to normal sequence. The mutation is near the 3′ end of exon 25. The exon/intron junction is indicated by the dashed line. (C) Cross-species alignment of the amino acid sequence surrounding residue L1165. (D) Cross-species alignment of the amino acid sequence surrounding residue R793.

Jason P. Covy, et al. Mov Disord. ;24(1):32-39.

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