Amyloid beta accumulation in HIV-1-infected brain: The role of the blood brain barrier

被引:53
|
作者
Andras, Ibolya E. [1 ]
Toborek, Michal [1 ]
机构
[1] Univ Miami, Sch Med, Dept Biochem & Mol Biol, Miami, FL 33136 USA
基金
美国国家卫生研究院;
关键词
HIV-1; HIV-1-associated neurocognitive disorders; blood-brain barrier; brain endothelial cell; amyloid beta; GLYCATION END-PRODUCTS; RECEPTOR-RELATED PROTEIN-1; TAT-INDUCED ALTERATIONS; ALZHEIMERS-DISEASE; P-GLYCOPROTEIN; AIDS PATIENTS; LDL RECEPTOR; LIPID RAFTS; HIV-1; EXPRESSION;
D O I
10.1002/iub.1106
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
In recent years, we face an increase in the aging of the HIV-1-infected population, which is not only due to effective antiretroviral therapy but also to new infections among older people. Even with the use of the antiretroviral therapy, HIV-associated neurocognitive disorders represent an increasing problem as the HIV-1-infected population ages. Increased amyloid beta (A beta) deposition is characteristic of HIV-1-infected brains, and it has been hypothesized that brain vascular dysfunction contributes to this phenomenon, with a critical role suggested for the blood-brain barrier in brain A beta homeostasis. This review will describe the mechanisms by which the blood-brain barrier may contribute to brain A beta accumulation, and our findings in the context of HIV-1 infection will be discussed. (c) 2012 IUBMB Life, 65(1):4349, 2013
引用
收藏
页码:43 / 49
页数:7
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