Implication of Complement System and its Regulators in Alzheimer's Disease

被引：1

作者：

Kolev, Martin V. ^{[1
]}

Ruseva, Marieta M. ^{[1
]}

Harris, Claire L. ^{[1
]}

Morgan, B. Paul ^{[1
]}

Donev, Rossen M. ^{[1
]}

机构：

[1] Cardiff Univ, Dept Med Biochem & Immunol, Sch Med, Cardiff CF14 4XN, S Glam, Wales

来源：

CURRENT NEUROPHARMACOLOGY | 2009年 / 7卷 / 01期

基金：

英国惠康基金; 英国医学研究理事会;

关键词：

Alzheimer's disease; neurodegeneration; inflammation; beta-amyloid peptide; complement; complement regulators; CD59; complement therapeutics; MANNAN-BINDING LECTIN; MEMBRANE ATTACK COMPLEX; AMYLOID-P COMPONENT; SEE VOL. 73; TRANSGENIC MODEL; EXPRESSION; CD59; PROTEIN; ACTIVATION; BRAIN;

D O I：

暂无

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer's disease (AD) is an age-related neurodegenerative disease that affects approximately 24 million people worldwide. A number of different risk factors have been implicated in AD, however, neuritic (amyloid) plaques are considered as one of the defining risk factors and pathological hallmarks of the disease. Complement proteins are integral components of amyloid plaques and cerebral vascular amyloid in Alzheimer brains. They can be found at the earliest stages of amyloid deposition and their activation coincides with the clinical expression of Alzheimer's dementia. This review emphasizes on the dual key roles of complement system and complement regulators (CRegs) in disease pathology and progression. The particular focus of this review is on currently evolving strategies for design of complement inhibitors that might aid therapy by restoring the fine balance between activated components of complement system, thus improving the cognitive performance of patients. This review discusses these issues with a view to inspiring the development of new agents that could be useful for the treatment of AD.

引用

页码：1 / 8

页数：8

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