AMYLOID-BETA PEPTIDE INDUCES CYTOPLASMIC ACCUMULATION OF AMYLOID PROTEIN-PRECURSOR VIA TAU-PROTEIN KINASE-I GLYCOGEN-SYNTHASE KINASE-3-BETA IN RAT HIPPOCAMPAL-NEURONS

被引：58

作者：

TAKASHIMA, A ^{[1
]}

YAMAGUCHI, H ^{[1
]}

NOGUCHI, K ^{[1
]}

MICHEL, G ^{[1
]}

ISHIGURO, K ^{[1
]}

SATO, K ^{[1
]}

HOSHINO, T ^{[1
]}

HOSHI, M ^{[1
]}

IMAHORI, K ^{[1
]}

机构：

[1] GUNMA UNIV, COLL MED CARE & TECHNOL, MAEBASHI, GUMMA 371, JAPAN

来源：

NEUROSCIENCE LETTERS | 1995年 / 198卷 / 02期

关键词：

AMYLOID BETA PROTEIN; AMYLOID PROTEIN PRECURSOR; ALZHEIMERS; NEUROFIBRILLARY TANGLES; PAIRED HELICAL FILAMENTS; TAU PROTEIN KINASE I GLYCOGEN SYNTHASE KINASE-3-BETA;

D O I：

10.1016/0304-3940(95)11964-X

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Exogenous application of synthetic amyloid beta protein (A beta) is known to induce neurotoxic effects in rat hippocampal culture. We report here that A beta (25-35) induces accumulation of amyloid precursor protein (APP) derivatives in the cytoplasm of neurons. At the same time, the level of the secreted form of APP released into the culture medium decreases. Tau protein kinase I/glycogen synthase kinase-3 beta (TPK I/GSK-3 beta) antisense oligonucleotide blocked APP accumulation and prevented neuronal death. These results provide evidence that APP accumulation after A beta treatment is regulated by TPK I/GSK-3 beta. A beta neurotoxicity is probably mediated via phosphorylation of tau by TPK I/GSK-3 beta, resulting in an impairment of axonal transport, and cytoplasmic accumulation of APP.

引用

页码：83 / 86

页数：4

共 22 条

[11] INTERACTION OF BETA-AMYLOID PEPTIDES WITH INTEGRINS IN A HUMAN NERVE-CELL LINE [J].

SABO, S ;

LAMBERT, MP ;

KESSEY, K ;

WADE, W ;

KRAFFT, G ;

KLEIN, WL .

NEUROSCIENCE LETTERS, 1995, 184 (01) :25-28

[12] AMYLOID BETA-PROTEIN PRECURSOR ACCUMULATES IN DYSTROPHIC NEURITES OF SENILE PLAQUES IN ALZHEIMER-TYPE DEMENTIA [J].

SHOJI, M ;

HIRAI, S ;

YAMAGUCHI, H ;

HARIGAYA, Y ;

KAWARABAYASHI, T .

BRAIN RESEARCH, 1990, 512 (01) :164-168

[13]

SISODIA SS, 1993, J NEUROSCI, V13, P3136

[14] MOLECULAR-CLONING OF THE CDNA FOR A HUMAN AMYLOID PRECURSOR PROTEIN HOMOLOG - EVIDENCE FOR A MULTIGENE FAMILY [J].

SPRECHER, CA ;

GRANT, FJ ;

GRIMM, G ;

OHARA, PJ ;

NORRIS, F ;

NORRIS, K ;

FOSTER, DC .

BIOCHEMISTRY, 1993, 32 (17) :4481-4486

[15] TAU-PROTEIN KINASE-I IS ESSENTIAL FOR AMYLOID BETA-PROTEIN-INDUCED NEUROTOXICITY [J].

TAKASHIMA, A ;

NOGUCHI, K ;

SATO, K ;

HOSHINO, T ;

IMAHORI, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (16) :7789-7793

[16]

TAKASHIMA A, UNPUB AMYLOID BETA P

[17] DECREASED LEVELS OF SOLUBLE AMYLOID BETA-PROTEIN PRECURSOR IN CEREBROSPINAL-FLUID OF LIVE ALZHEIMER-DISEASE PATIENTS [J].

VANNOSTRAND, WE ;

WAGNER, SL ;

SHANKLE, WR ;

FARROW, JS ;

DICK, M ;

ROZEMULLER, JM ;

KUIPER, MA ;

WOLTERS, EC ;

ZIMMERMAN, J ;

COTMAN, CW ;

CUNNINGHAM, DD .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (07) :2551-2555

[18] HUMAN NEURONS DERIVED FROM A TERATOCARCINOMA CELL-LINE EXPRESS SOLELY THE 695-AMINO ACID AMYLOID PRECURSOR PROTEIN AND PRODUCE INTRACELLULAR BETA-AMYLOID OR A4 PEPTIDES [J].

WERTKIN, AM ;

TURNER, RS ;

PLEASURE, SJ ;

GOLDE, TE ;

YOUNKIN, SG ;

TROJANOWSKI, JQ ;

LEE, VMY .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (20) :9513-9517

[19] NEUROTOXICITY OF A FRAGMENT OF THE AMYLOID PRECURSOR ASSOCIATED WITH ALZHEIMERS-DISEASE [J].

YANKNER, BA ;

DAWES, LR ;

FISHER, S ;

VILLAKOMAROFF, L ;

OSTERGRANITE, ML ;

NEVE, RL .

SCIENCE, 1989, 245 (4916) :417-420

[20] NEUROTROPHIC AND NEUROTOXIC EFFECTS OF AMYLOID BETA-PROTEIN - REVERSAL BY TACHYKININ NEUROPEPTIDES [J].

YANKNER, BA ;

DUFFY, LK ;

KIRSCHNER, DA .

SCIENCE, 1990, 250 (4978) :279-282

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