Tau aggregation into fibrillar polymers: taupathies

被引：76

作者：

Avila, J ^{[1
]}

机构：

[1] Univ Autonoma Madrid, Fac Ciencias, CSIC, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain

来源：

FEBS LETTERS | 2000年 / 476卷 / 1-2期

关键词：

tau protein; assembly; neurodegeneration; Alzheimer's disease;

D O I：

10.1016/S0014-5793(00)01676-8

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Different neurological disorders, known as taupathies have been recently described. In these disorders it has been suggested that modifications in the microtubule-associated protein tau could cause neural degeneration in specific regions. Although these regions are different in the different taupathies, some common features appear to occur in all of them: abnormal hyperphosphorylation of tau and aberrant tau aggregation. These two features are commented upon in this review. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：89 / 92

页数：4

共 60 条

[1] Abnormal phosphorylation of tan and the mechanism of Alzheimer neurofibrillary degeneration: Sequestration of microtubule-associated proteins 1 and 2 and the disassembly of microtubules by the abnormal tau [J].

Alonso, AD ;

GrundkeIqbal, I ;

Barra, HS ;

Iqbal, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (01) :298-303

[2] Lithium protects cultured neurons against β-amyloid-induced neurodegeneration [J].

Alvarez, G ;

Muñoz-Montaño, JR ;

Satrústegui, J ;

Avila, J ;

Bogónez, E ;

Díaz-Nido, J .

FEBS LETTERS, 1999, 453 (03) :260-264

[3] Alzheimer's disease: Clues from flies and worms [J].

Anderton, BH .

CURRENT BIOLOGY, 1999, 9 (03) :R106-R109

[4] Polymerization of tau peptides into fibrillar structures.: The effect of FTDP-17 mutations [J].

Arrasate, M ;

Pérez, M ;

Armas-Portela, R ;

Avila, J .

FEBS LETTERS, 1999, 446 (01) :199-202

[5]

Arrasate M, 1997, AM J PATHOL, V151, P1115

[6] NEUROFIBRILLARY TANGLES BUT NOT SENILE PLAQUES PARALLEL DURATION AND SEVERITY OF ALZHEIMERS-DISEASE [J].

ARRIAGADA, PV ;

GROWDON, JH ;

HEDLEYWHYTE, ET ;

HYMAN, BT .

NEUROLOGY, 1992, 42 (03) :631-639

[7] NEUROFIBRILLARY DEGENERATION AND NEURONAL LOSS IN ALZHEIMERS-DISEASE [J].

BONDAREFF, W ;

MOUNTJOY, CQ ;

ROTH, M ;

HAUSER, DL .

NEUROBIOLOGY OF AGING, 1989, 10 (06) :709-715

[8] MOLECULAR CHANGES IN SENILE DEMENTIA [J].

BOWEN, DM ;

SMITH, CB ;

DAVISON, AN .

BRAIN, 1973, 96 (DEC) :849-856

[9] A SEQUENCE OF CYTOSKELETON CHANGES RELATED TO THE FORMATION OF NEUROFIBRILLARY TANGLES AND NEUROPIL THREADS [J].

BRAAK, E ;

BRAAK, H ;

MANDELKOW, EM .

ACTA NEUROPATHOLOGICA, 1994, 87 (06) :554-567

[10] Frequency of stages of Alzheimer-related lesions in different age categories [J].

Braak, H ;

Braak, E .

NEUROBIOLOGY OF AGING, 1997, 18 (04) :351-357

← 1 2 3 4 5 6 →