Abeta Amyloidosis Induces the Initial Stage of Tau Accumulation in APP(Sw) Mice

Overview

Journal Neurosci Lett

Specialty Neurology

Date 2001 Feb 13

PMID 11165762

Citations 19

Authors

Y Tomidokoro

K Ishiguro

Y Harigaya

E Matsubara

M Ikeda

J M Park

K Yasutake

T Kawarabayashi

K Okamoto

M Shoji

Affiliations

Soon will be listed here.

Abstract

To clarify how Abeta deposits induce secondary tauopathy, the presence of phosphorylated tau, glycogen synthase kinase 3alpha (GSK3alpha), GSK3beta, cyclin-dependent kinase 5 (CDK5), mitogen-activated protein kinase (MAPK) and fyn were examined in the Tg2576 brain showing substantial brain Abeta amyloidosis and behavioral abnormalities. Phosphorylated tau at Ser199, Thr231/Ser235, Ser396 and Ser413 accumulated in the dystrophic neurites of senile plaques. The major kinase for tau phosphorylation was GSK3beta. Smaller contributions of GSK3alpha, CDK5 and MAPK were suggested. Thus, brain Abeta amyloidosis has a potential role in the induction of tauopathy leading to the mental disturbances of Alzheimer's disease.

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