Cytokines in neuroinflammation and Alzheimer's disease

被引：196

作者：

Cacquevel, M ^{[1
]}

Lebeurrier, N ^{[1
]}

Chéenne, S ^{[1
]}

Vivien, D ^{[1
]}

机构：

[1] Univ Caen, UMR 6185, CNRS, Ctr Cyceron, F-14074 Caen, France

来源：

CURRENT DRUG TARGETS | 2004年 / 5卷 / 06期

关键词：

Alzheimer's disease; inflammation; cytokine; TGF-beta;

D O I：

10.2174/1389450043345308

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Inflammation has been reported in numerous neurodegenerative disorders such as Parkinson's disease. stroke and Alzheimer's disease (AD). In AD, the inflammatory response is mainly located to the vicinity of amlyloid plaques. Cytokines, such as Interleukin-1 (IL-1), Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-alpha) and Transforming Growth Factor beta (TGF-beta) have been clearly involved in this inflammatory process. Although their expression is induced by the presence of amyloid-beta peptide, these cytokines are also able to promote the accumulation of amyloid-beta peptide. Altogether, IL-1, IL-6, TNF-alpha and TGT-beta should be considered as key players of a vicious circle leading to the progression of the disease.

引用

页码：529 / 534

页数：6

共 115 条

[1] β-amyloid stimulation of inducible nitric-oxide synthase in astrocytes is interleukin-1β- and tumor necrosis factor-α (TNFα)-dependent, and involves a TNFα receptor-associated factor- and NFκB-inducing kinase-dependent signaling mechanism [J].

Akama, KT ;

Van Eldik, LJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (11) :7918-7924

[2]

ALOISI F, 1992, J IMMUNOL, V149, P2358

[3] Association between the TNFα-308 A/G polymorphism and the onset-age of Alzheimer disease [J].

Alvarez, V ;

Mata, IF ;

González, P ;

Lahoz, CH ;

Martínez, C ;

Peña, J ;

Guisasola, LM ;

Coto, E .

AMERICAN JOURNAL OF MEDICAL GENETICS, 2002, 114 (05) :574-577

[4] TGF-β1, regulation of Alzheimer amyloid precursor protein mRNA expression in a normal human astrocyte cell line:: mRNA stabilization [J].

Amara, FM ;

Junaid, A ;

Clough, RR ;

Liang, BH .

MOLECULAR BRAIN RESEARCH, 1999, 71 (01) :42-49

[5] Oxidative signalling and inflammatory pathways in Alzheimer's disease [J].

Anderson, I ;

Adinolfi, C ;

Doctrow, S ;

Huffman, K ;

Joy, KA ;

Malfroy, B ;

Soden, P ;

Rupniak, HT ;

Barnes, JC .

NEURONAL SIGNAL TRANSDUCTION AND ALZHEIMER'S DISEASE, 2001, 67 :141-149

[6] Serum interleukin-6 and interleukin-6 soluble receptor in Alzheimer's disease [J].

Angelis, P ;

Scharf, S ;

Mander, A ;

Vajda, F ;

Christophidis, N .

NEUROSCIENCE LETTERS, 1998, 244 (02) :106-108

[7] β-Amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology [J].

Apelt, J ;

Schliebs, R .

BRAIN RESEARCH, 2001, 894 (01) :21-30

[8] Association study of three polymorphisms of TGF-β1 gene with Alzheimer's disease [J].

Araria-Goumidi, L ;

Lambert, JC ;

Mann, DMA ;

Lendon, C ;

Frigard, B ;

Iwatsubo, T ;

Cottel, D ;

Amouyel, P ;

Chartier-Harlin, MC .

JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 2002, 73 (01) :62-64

[9] BETA-AMYLOID STIMULATES GLIAL-CELLS INVITRO TO PRODUCE GROWTH-FACTORS THAT ACCUMULATE IN SENILE PLAQUES IN ALZHEIMERS-DISEASE [J].

ARAUJO, DM ;

COTMAN, CW .

BRAIN RESEARCH, 1992, 569 (01) :141-145

[10] Interleukin-1 receptor antagonist: Role in biology [J].

Arend, WP ;

Malyak, M ;

Guthridge, CJ ;

Gabay, C .

ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 :27-55

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