Results: 5

1.
Fig. 2

Fig. 2. From: A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain.

OC immunolabeling is distinct from thioflavine S-positive fibrils within plaques and also identifies diffuse plaque deposits. OC-positive deposits (a) had a distinct morphology that appears as shorter aggregates (red) as compared to thioflavine S-positive fibrils (green) (b). Further, when OC and thioflavine-S was colocalized within plaques (orange), OC labeling was more intense in the periphery (c). Using tissue from a nondemented elderly subject (df) and a younger individual with DS (gi), both having primarily diffuse plaques (thioflavine S-negative—green), we observed that diffuse plaques are also OC-positive (red). A z-scan shows that OC-positive deposits (green) could also be distinguished from A11-positive oligomers (red) in mature plaques observed in DS frontal cortex

Floyd Sarsoza, et al. Acta Neuropathol. 2009 October;118(4):505-517.
2.
Fig. 3

Fig. 3. From: A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain.

Characteristics of OC-positive deposits. A subset of OC deposits (red) contained dystrophic neurites labeled by PHF (green arrows) that could be distinguished from tangle bearing neurons (arrowheads) (a). Not all OC (red) deposits contained PHF positive dystrophic neurites (green) (b). Dystrophic neurites labeled with ubiquitin (green) were also found in association with a subset of OC deposits (red) (c). A subset of OC (red) deposits was associated with activated microglial (LN-3 green) (d) Area in d indicated by asterisk at higher magnification illustrating two activated microglial cells (green) surrounding an OC-positive deposit (red) (e). A subset of activated microglial cells (green) appear to have engulfed OC-positive material (arrows red/orange) whereas other microglial cells appear OC-negative (arrowhead) (f). OC-positive deposits (red) are surrounded by astrocytes (green) (g). A higher magnification of the region in g indicated by the asterisk shows that some astrocytes in proximity to OC appear hypertrophied (h)

Floyd Sarsoza, et al. Acta Neuropathol. 2009 October;118(4):505-517.
3.
Fig. 1

Fig. 1. From: A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain.

Formic acid pretreatment has little effect on OC labeling intensity. Increasing concentrations of formic acid pretreatment (a none, b 10%, c 50%, d 70%, e 90%) were used in an AD case (frontal cortex) to illustrate no change in OC (red fluorescence) immunolabeling but an increase in 6E10 (green fluorescence) labeling. Note that with increasing formic acid and corresponding increase in 6E10 labeling, the extent of co-localization of the two markers also increases (orange fluorescence). In comparison, a control case shows neither significant OC nor 6E10 immunolabeling (f). However, a subset of OC-positive deposits (g and i) was negative for 6E10 (h and i)

Floyd Sarsoza, et al. Acta Neuropathol. 2009 October;118(4):505-517.
4.
Fig. 5

Fig. 5. From: A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain.

OC fibril labeling in Tg2576 animals. a Tg2576 animals show increasing OC accumulation with age while no OC was observed in comparably aged wild type animals. OC loads were obtained from the b frontoparietal cortex, c entorhinal cortex and d from area CA1 in the hippocampus of individual animals. Mean loads are plotted as a function of age for each brain region and show a dramatic increase after 12 months of age in cortical regions but with a slower more progressive rise in the hippocampus. Error bars represent standard errors of the mean (n = 5 animals/age group)

Floyd Sarsoza, et al. Acta Neuropathol. 2009 October;118(4):505-517.
5.
Fig. 4

Fig. 4. From: A fibril-specific, conformation-dependent antibody recognizes a subset of Aβ plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain.

The extent of OC labeling in AD and DS brain. More extensive OC immunoreactivity was observed in the AD cases relative to both the control and MCI/CIND cases (a). Higher MMSE scores were associated with less extensive OC immunolabeling (r = −0.72, p < 0.001) (b). In DS cases used in experiment 2, OC labeling appears to be significantly reduced when the PMI is over 10 h (c). A significant increase in OC was observed in adults with DS over the age of 40 years (open circlesd) but not in similarly aged non-DS controls (closed circles). When OC loads are plotted as a function of individual age, there is an exponential rise in Aβ fibril accumulation after the age of 40 years in DS (open circles) but not in non-DS controls (closed circles) (d). Bars represent means and error bars, standard errors of the mean. In bd, the lines represent a best fit function

Floyd Sarsoza, et al. Acta Neuropathol. 2009 October;118(4):505-517.

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