Abstract：
: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.
journal_name
Brain Resjournal_title
Brain researchauthors
Samura E,Shoji M,Kawarabayashi T,Sasaki A,Matsubara E,Murakami T,Wuhua X,Tamura S,Ikeda M,Ishiguro K,Saido TC,Westaway D,St George Hyslop P,Harigaya Y,Abe Kdoi
10.1016/j.brainres.2005.12.134subject
Has Abstractpub_date
2006-06-13 00:00:00pages
192-9issue
1eissn
0006-8993issn
1872-6240pii
S0006-8993(06)00616-0journal_volume
1094pub_type
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