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Rather, an influence of pre-existing plaques was necessary to successfully model the spatial pattern of plaque formation in AD pathology.
An alternative model proposed that random spatial allocation was not sufficient to match the pattern of plaque distribution found in post-mortem histological tissue, but rather that plaques favorably emerged in the vicinity of an already existing plaque [ 32].
Thus, the timing and pattern of plaque distribution after microinjection of tg44 mice with RML scrapie supported our previous hypothesis that spread of infectivity occurred via dissemination with brain interstitial fluid (ISF) in perivascular regions of gray and white matter and in interaxonal spaces of white matter tracts [ 31].
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The architectural pattern of plaques also varied between different anatomic regions.
Furthermore, in each individual the architectural pattern of plaques was found to vary between different anatomic regions from diffuse deposits to targetoid or ring-shaped plaques.
Therefore, although our analysis included prospective cohort data, we cannot account for potential changes in patterns of plaque scores and serum albumin levels during the 5-year follow-up period.
In this study, we aimed to compare the presence, locations, and contrast-enhanced patterns of plaques on the ipsilateral and contralateral side of the RSSI using contrast-enhanced three-dimensional HR-MRI (3D HR-MRI).
The purpose of this study was to describe the pattern of dental plaque accumulation in mechanically ventilated adults.
Corneal epithelial tissue grown on polycarbonate surfaces with pore diameters of 0.1 3.0 μm were shown to lay down continuous BM and a regular pattern of hemidesmosomal plaque on a 0.1 μm surface, and no adhesive structures assembled on a nonporous or 3.0 μm surface [42].
Recently, several studies have described specific attenuation pattern of atherosclerotic plaques on coronary CT images characterized by a plaque core with low CT attenuation surrounded by a rim-like area of higher CT attenuation as napkin-ring sign [ 79– 81].
Interestingly, the plaque morphology, distribution pattern and sequence of plaque formation in ARTE10 mice are relatively similar to some of the other APP and presenilin expressing mouse lines, although in some cases different promoters and even different APP and/or presenilin mutants have been used [2], [4], [25], [26].
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