Dysregulation of protein phosphorylation/dephosphorylation in Alzheimer's disease: A therapeutic target

被引：58

作者：

Gong, Cheng-Xin ^{[1
]}

Liu, Fei ^{[1
]}

Grundke-Iqbal, Inge ^{[1
]}

Iqbal, Khalid ^{[1
]}

机构：

[1] New York State Inst Basic Res Dev Disabil, Dept Neurochem, Staten Isl, NY 10314 USA

来源：

JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY | 2006年

关键词：

D O I：

10.1155/JBB/2006/31825

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Studies during the last two decades have provided new insights into the molecular mechanism of Alzheimer's disease ( AD). One of the milestone findings in AD research was the demonstration that neurofibrillary degeneration characterized by tau pathology is central to the pathogenesis of AD and other tauopathies and that abnormal hyperphosphorylation of tau is pivotal to neurofibrillary degeneration. This article reviews the recent research advances in tau pathology and the underlying dysregulation of the protein phosphorylation/dephosphorylation system. An updated model of the mechanism of neurofibrillary degeneration is also presented, and a promising therapeutic target to treat AD by correcting dysregulation of protein phosphorylation/ dephosphorylation is discussed.

引用

页数：11

共 159 条

[61]

IQBAL K, 1986, LANCET, V2, P421

[62] Tau pathology in Alzheimer disease and other tauopathies [J].

Iqbal, K ;

Alonso, ADC ;

Chen, S ;

Chohan, MO ;

El-Akkad, E ;

Gong, CX ;

Khatoon, S ;

Li, B ;

Liu, F ;

Rahman, A ;

Tanimukai, H ;

Grundke-Iqbal, I .

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2005, 1739 (2-3) :198-210

[63] ALZHEIMER PAIRED HELICAL FILAMENTS - RESTORATION OF THE BIOLOGICAL-ACTIVITY BY DEPHOSPHORYLATION [J].

IQBAL, K ;

ZAIDI, T ;

BANCHER, C ;

GRUNDKEIQBAL, I .

FEBS LETTERS, 1994, 349 (01) :104-108

[64] Phosphorylated tau in human cerebrospinal fluid is a diagnostic marker for Alzheimer's disease [J].

Ishiguro, K ;

Ohno, H ;

Arai, H ;

Yamaguchi, H ;

Urakami, K ;

Park, JM ;

Sato, K ;

Kohno, H ;

Imahori, K .

NEUROSCIENCE LETTERS, 1999, 270 (02) :91-94

[65] Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform [J].

Ishihara, T ;

Hong, M ;

Zhang, B ;

Nakagawa, Y ;

Lee, MK ;

Trojanowski, JQ ;

Lee, VMY .

NEURON, 1999, 24 (03) :751-762

[66] Large-scale, multicenter study of cerebrospinal fluid tau protein phosphorylated at serine 199 for the antemortem diagnosis of Alzheimer's disease [J].

Itoh, N ;

Arai, H ;

Urakami, K ;

Ishiguro, K ;

Ohno, H ;

Hampel, H ;

Buerger, K ;

Wiltfang, J ;

Otto, M ;

Kretzschmar, H ;

Moeller, HJ ;

Imagawa, M ;

Kohno, H ;

Nakashima, K ;

Kuzuhara, S ;

Sasaki, H ;

Imahori, K .

ANNALS OF NEUROLOGY, 2001, 50 (02) :150-156

[67] Human wild-type tau interacts with wingless pathway components and produces neurofibrillary pathology in Drosophila [J].

Jackson, GR ;

Wiedau-Pazos, M ;

Sang, TK ;

Wagle, N ;

Brown, CA ;

Massachi, S ;

Geschwind, DH .

NEURON, 2002, 34 (04) :509-519

[68] MYOTONIC-DYSTROPHY - CORRELATION OF CLINICAL SYMPTOMS WITH THE SIZE OF THE CTG TRINUCLEOTIDE REPEAT [J].

JASPERT, A ;

FAHSOLD, R ;

GREHL, H ;

CLAUS, D .

JOURNAL OF NEUROLOGY, 1995, 242 (02) :99-104

[69] Tau complexes with phospholipase C-γ in situ [J].

Jenkins, SM ;

Johnson, GVW .

NEUROREPORT, 1998, 9 (01) :67-71

[70] Tau phosphorylation in neuronal cell function and dysfunction [J].

Johnson, GVW ;

Stoothoff, WH .

JOURNAL OF CELL SCIENCE, 2004, 117 (24) :5721-5729

← 2 3 4 5 6 7 8 9 10 11 →