| First Author | Samura E | Year | 2006 |
| Journal | Brain Res | Volume | 1094 |
| Issue | 1 | Pages | 192-9 |
| PubMed ID | 16713590 | Mgi Jnum | J:110440 |
| Mgi Id | MGI:3640234 | Doi | 10.1016/j.brainres.2005.12.134 |
| Citation | Samura E, et al. (2006) Enhanced accumulation of tau in doubly transgenic mice expressing mutant betaAPP and presenilin-1. Brain Res 1094(1):192-9 |
| abstractText | Abeta amyloidosis and tauopathy are characteristic changes in the brain of Alzheimer's disease. Although much evidence suggests that Abeta deposit is a critical initiation factor, the pathological pathway between Abeta amyloidosis and tau accumulation remains unclear. Tau accumulation was examined in the doubly transgenic mouse (APP-PS) expressing betaAPP(KM670/671NL) (Tg2576) and presenilin-1 L286V (PS-1 L286Vtg). Accelerated and enhanced Abeta amyloid deposits were detected from 8 weeks. Tau accumulation appeared at 4.5 months and markedly increased in dystrophic neurites around Abeta amyloid. Accumulated tau was phosphorylated, conformationally altered, and argyrophilic. Expression of tau and accumulation of sarkosyl-insoluble phosphorylated tau were increased in APP-PS brains compared with those of Tg2576 mice. Straight or twisted tubules mimicking paired helical filament were revealed at electron microscopic level in 16-month-old APP-PS. These findings suggest that mutant presenilin-1 accelerated Abeta-induced tauopathy and further promoted fibril formation of tau. |
