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O4‐06‐03: Aβ/APP‐dependent tangle modification via WAVE accumulation in Alzheimer's disease
Author(s) -
Takata Kazuyuki,
Kitamura Yoshihisa,
Matsuoka Yasuji,
Shimohama Shun,
Taniguchi Takashi
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.498
Subject(s) - neurite , phosphorylation , tau protein , microbiology and biotechnology , senile plaques , chemistry , amyloid precursor protein , neurofibrillary tangle , alzheimer's disease , genetically modified mouse , neuroscience , biology , pathology , transgene , biochemistry , medicine , disease , in vitro , gene
dual-labeling immuno-EM. High resolution 3D images showed that intracellular thioflavin S staining was evident within selective pyramidal neurons and neurites in Tg19959 mouse brain (Figure, arrows). Increasing intracellular thioflavin S staining intensity correlated inversely with intraneuronal SMI32 neurofilament labeling (Figure, arrowhead). Conclusions: We provide further data demonstrating that Ab accumulation, oligomerization and fibrilization initially begins within AD vulnerable neurons. The progressive aggregation of Ab42 particularly within neurites leads directly to disruption of the cytoarchitecture (evidenced by loss of MAP2 and SMI32) and degeneration of neurites, providing the nidus for plaque formation.