| First Author | Hashimoto T | Year | 2020 |
| Journal | Acta Neuropathol Commun | Volume | 8 |
| Issue | 1 | Pages | 212 |
| PubMed ID | 33287899 | Mgi Jnum | J:313968 |
| Mgi Id | MGI:6801201 | Doi | 10.1186/s40478-020-01075-5 |
| Citation | Hashimoto T, et al. (2020) Collagenous Alzheimer amyloid plaque component impacts on the compaction of amyloid-beta plaques. Acta Neuropathol Commun 8(1):212 |
| abstractText | Massive deposition of amyloid beta peptides (Abeta) as senile plaques (SP) characterizes the brain pathology of Alzheimer's disease (AD). SPs exhibit a variety of morphologies, although little is known about the SP components that determine their morphology. Collagenous Alzheimer amyloid plaque component (CLAC) is one of the major non-Abeta proteinaceous components of SP amyloid in AD brains. Here we show that overexpression of CLAC precursor (CLAC-P) in the brains of APP transgenic mice results in a significant remodeling of amyloid pathology, i.e., reduction in diffuse-type amyloid plaques and an increase in compact plaques laden with thioflavin S-positive amyloid cores. In vivo microdialysis revealed a significant decrease in Abeta in the brain interstitial fluid of CLAC-P/APP double transgenic mice compared with APP transgenic mice. These findings implicate CLAC in the compaction of Abeta in amyloid plaques and the brain dynamics of Abeta. |
