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Enhanced accumulation of tau in doubly transgenic mice expressing mutant betaAPP and presenilin-1.
Brain Res 2006; 1094(1):192-9BR

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.

Authors+Show Affiliations

Department of Neurology, Division of Neuroscience, Biophysical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16713590

Citation

Samura, Eriko, et al. "Enhanced Accumulation of Tau in Doubly Transgenic Mice Expressing Mutant betaAPP and Presenilin-1." Brain Research, vol. 1094, no. 1, 2006, pp. 192-9.
Samura E, Shoji M, Kawarabayashi T, et al. Enhanced accumulation of tau in doubly transgenic mice expressing mutant betaAPP and presenilin-1. Brain Res. 2006;1094(1):192-9.
Samura, E., Shoji, M., Kawarabayashi, T., Sasaki, A., Matsubara, E., Murakami, T., ... Abe, K. (2006). Enhanced accumulation of tau in doubly transgenic mice expressing mutant betaAPP and presenilin-1. Brain Research, 1094(1), pp. 192-9.
Samura E, et al. Enhanced Accumulation of Tau in Doubly Transgenic Mice Expressing Mutant betaAPP and Presenilin-1. Brain Res. 2006 Jun 13;1094(1):192-9. PubMed PMID: 16713590.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enhanced accumulation of tau in doubly transgenic mice expressing mutant betaAPP and presenilin-1. AU - Samura,Eriko, AU - Shoji,Mikio, AU - Kawarabayashi,Takeshi, AU - Sasaki,Atsushi, AU - Matsubara,Etsuro, AU - Murakami,Tetsuro, AU - Wuhua,Xu, AU - Tamura,Shuta, AU - Ikeda,Masaki, AU - Ishiguro,Koich, AU - Saido,Takaomi C, AU - Westaway,David, AU - St George Hyslop,Peter, AU - Harigaya,Yasuo, AU - Abe,Koji, Y1 - 2006/05/19/ PY - 2005/08/01/received PY - 2005/12/22/revised PY - 2005/12/27/accepted PY - 2006/5/23/pubmed PY - 2006/9/19/medline PY - 2006/5/23/entrez SP - 192 EP - 9 JF - Brain research JO - Brain Res. VL - 1094 IS - 1 N2 - 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. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/16713590/Enhanced_accumulation_of_tau_in_doubly_transgenic_mice_expressing_mutant_betaAPP_and_presenilin_1_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(06)00616-0 DB - PRIME DP - Unbound Medicine ER -