Current insights into apolipoprotein E and the immune response in Alzheimer's disease

被引：1

作者：

Lin, Peter Bor-Chian ^{[1
]}

Holtzman, David M. ^{[1
]}

机构：

[1] Washington Univ, Hope Ctr Neurol Disorders, Knight Alzheimers Dis Res Ctr, Dept Neurol, St Louis, MO 63130 USA

来源：

IMMUNOLOGICAL REVIEWS | 2024年 / 327卷 / 01期

基金：

美国国家卫生研究院;

关键词：

Alzheimer's disease; apolipoprotein E; immune responses; LOW-DENSITY LIPOPROTEINS; TRIGLYCERIDE-RICH LIPOPROTEINS; TAU-MEDIATED NEURODEGENERATION; CYSTEINE-ARGININE INTERCHANGE; REDUCES AMYLOID DEPOSITION; RECEPTOR-BINDING ACTIVITY; MOUSE MODEL; PERIPHERAL-TISSUES; PLAQUE-FORMATION; TERMINAL DOMAIN;

D O I：

10.1111/imr.13414

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Alzheimer's disease (AD) is a progressive neurological disorder and the most common cause of dementia. Genetic analyses identified apolipoprotein E (APOE) as the strongest genetic risk for late-onset AD. Studies have shown that ApoE modulates AD pathogenesis in part by influencing amyloid-beta (A beta) deposition. However, ApoE also appears to regulate elements of AD via regulation of innate immune response, especially through microglial and astrocyte activation. In model systems, it also regulates changes in T-cells. This review focuses on the key findings that have advanced our understanding of the role of ApoE in the pathogenesis of AD and the current view of innate immune response regulated by ApoE in AD, while discussing open questions and areas for future research.

引用

页码：43 / 52

页数：10

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