GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
TableEdit
PMID:15215182
You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki
See Help for Help on this wiki. See the documentation for how to use the table editor
| Citation |
Kowa, H, Sakakura, T, Matsuura, Y, Wakabayashi, T, Mann, DM, Duff, K, Tsuji, S, Hashimoto, T and Iwatsubo, T (2004) Mostly separate distributions of CLAC- versus Abeta40- or thioflavin S-reactivities in senile plaques reveal two distinct subpopulations of beta-amyloid deposits. Am. J. Pathol. 165:273-81 |
|---|---|
| Abstract |
Collagenous Alzheimer amyloid plaque component (CLAC) is a unique non-Abeta amyloid component of senile plaques (SP) derived from a transmembrane collagen termed CLAC-precursor. Here we characterize the chronological and spatial relationship of CLAC with other features of SP amyloid in the brains of patients with Alzheimer's disease (AD), Down syndrome (DS), and of PSAPP transgenic mice. In AD and DS cerebral cortex, CLAC invariably colocalized with Abeta42 but often lacked Abeta40- or thioflavin S (thioS)-reactivities. Immunoelectron microscopy of CLAC-positive SP showed labeling of fibrils that are more loosely dispersed compared to typical amyloid fibrils in CLAC-negative SP. In DS cerebral cortex, diffuse plaques in young patients were negative for CLAC, whereas a subset of SP became CLAC-positive in patients aged 35 to 50 years, before the appearance of Abeta40. In DS cases over 50 years of age, Abeta40-positive SP dramatically increased, whereas CLAC burden remained at a constant level. In PSAPP transgenic mice, CLAC was positive in the diffuse Abeta deposits surrounding huge-cored plaques. Thus, CLAC and Abeta40 or thioS exhibit mostly separate distribution patterns in SP, suggesting that CLAC is a relatively early component of SP in human brains that may have inhibitory effects against the maturation of SP into beta-sheet-rich amyloid deposits. |
| Links | |
| Keywords |
Adult; Aged; Aged, 80 and over; Alzheimer Disease/metabolism; Alzheimer Disease/pathology; Amyloid beta-Peptides/metabolism; Animals; Antibodies, Monoclonal/metabolism; Down Syndrome/metabolism; Down Syndrome/pathology; Female; Fluorescent Antibody Technique, Indirect; Humans; Immunohistochemistry; Male; Membrane Proteins/metabolism; Membrane Proteins/ultrastructure; Mice; Mice, Transgenic; Middle Aged; Neocortex/cytology; Neocortex/metabolism; Neocortex/pathology; Neurons/metabolism; Neurons/pathology; Non-Fibrillar Collagens; Peptide Fragments/metabolism; Plaque, Amyloid/chemistry; Plaque, Amyloid/ultrastructure; Thiazoles/metabolism; Tissue Distribution |
| public |
| Cancel |
