Journal: Experimental Neurobiology

Article Title: An Autopsy-proven Case-based Review of Autoimmune Encephalitis

doi: 10.5607/en23036

Figure Lengend Snippet: (A, B) At autopsy, the brain weight was 1290 gm and mild global atrophy was seen. (C, D) The circle of Willis showed severe atherosclerosis with luminal occlusion in more than 50% of the lumen, which is severity score 3 according to the vascular cognitive impairment neuropathological guidline (VCING) criteria. (E) Luxol fast blue stain section showed hyalinization of arterioles with perivascular dilatation and white matter rarefaction, compatible with small vessel disease (arteriolosclerosis). There were corpora amylacea in the white matter adjacent to arteriosclerotic vessels, suggesting parenchymal damage by arteriolosclerosis. (F) Immunohistochemical analysis with phosphorylated tau revealed positive neurofibrillary tangles, neuropil threads in the temporal lobe (Braak stage III/VI), as well as classic amyloid cored plaques (shown in the inlet) that were present in the whole neocortex, hippocampus, thalamus, amygdala, basal ganglia, and midbrain (Thal phase was 4/5). Therefore, the patient had an intermediate level of Alzheimer’s neuropathologic change by neuropathological National Institute on Aging and the Alzheimer’s Association (NIA-AA) criteria (A3, B2, C2) (Under bar scale: D: 500 μm, E: 50 μm, F: 5 mm).

Article Snippet: The primary antibodies ( ) used in this study included NeuN (1:500, Millipore, Temecula, USA), synaptophysin (1:200, Novocastra, Neuwcastle, UK), GFAP (RTU, Ventana), Neurofilament (NF, 1:2000, DAKO, Glostrup, Denmark), CD3 (RTU, Ventana), CD8 (RTU, Ventana), CD20 (1:500, DAKO), CD68 (1:2000, DAKO), and TMEM119 (1:500, ABCAM, Bristol, UK), PD1, PDL-1 and stains for Luxol fast blue (LFB), myelin basic protein (MBP, 1:200, Cell Marque, Rocklin, US), aquaporin 4 (1:2000, Millipore), CMV (1:50, DAKO), and HSV (RTU, DAKO).

Techniques: Staining, Immunohistochemical staining

Journal: Magma (New York, N.Y.)

Article Title: Detection of axonal degeneration in a mouse model of Huntington’s disease: comparison between diffusion tensor imaging and anomalous diffusion metrics

doi: 10.1007/s10334-019-00742-6

Figure Lengend Snippet: Multi-cellular changes in the corpus callosum of the Huntington’s disease mice reveals increased white matter complexity. a Diagram showing coronal sections and histological regions of interest (ROIs in light blue) centered in the corpus callosum (CC) between the cortex (CCX) and the striatum. b Coronal sections centered in the corpus callosum showing changes in neuronal architecture and axonal orientation by endogenous expression. Yellow fluorescent protein (YFP) can be observed in the R6/2 mice (YFP, R6/2). Note an increase of axonal tortuosity in the R6/2 mice. Nuclear counterstaining with DAPI (Blue). Astrocyte proliferation is labeled by glial fibrillary acid protein (GFAP) and can be observed in white matter (WM) in the HD mice. The amount of myelin basic protein (MBP)—a marker of oligodendrocyte function—is decreased in the HD mice. c Quantitative fluorescence analysis of white matter markers (YFP, GFAP, and MBP) in the corpus callosum of the R6/2 and WT mice (***p < 0.001) (n = 6 mice per group). AU Arbitrary Units. Scale bar = 10 μm

Article Snippet: Sections were incubated with TBS containing primary antibodies recognizing myelin basic protein (MBP; PhosphoSolution, Cat #1120-MBP 1:500 Aurora, CO, USA) or the astrocyte maker glial fibrillary acid protein (GFAP; NeuroMab Cat #75–240 1:50, Davis, CA, USA).

Techniques: Expressing, Labeling, Marker, Fluorescence