Inflammatory aspects of Alzheimer's disease

被引:10
|
作者
Lucena, Pablo Botella [1 ]
Heneka, Michael T. [1 ,2 ]
机构
[1] Univ Luxembourg, Luxembourg Ctr Syst Biomed, 6 Ave Swing, L-4367 Belvaux, Esch Belval, Luxembourg
[2] Univ Massachusetts, Med Sch, Dept Infect Dis & Immunol, Worcester, MA 01605 USA
关键词
Innate immunity; Activation; Cytokine; Immune mediator; Neurodegeneration; Neuroinflammation; Alzheimer's disease; AMYLOID PRECURSOR PROTEIN; NF-KAPPA-B; TAU PATHOLOGY; NLRP3; INFLAMMASOME; RECEPTOR; A-BETA; ASTROCYTE REACTIVITY; BRAIN PERICYTES; GLOBAL BURDEN; MOUSE MODELS;
D O I
10.1007/s00401-024-02790-2
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Alzheimer<acute accent>s disease (AD) stands out as the most common chronic neurodegenerative disorder. AD is characterized by progressive cognitive decline and memory loss, with neurodegeneration as its primary pathological feature. The role of neuroinflammation in the disease course has become a focus of intense research. While microglia, the brain's resident macrophages, have been pivotal to study central immune inflammation, recent evidence underscores the contributions of other cellular entities to the neuroinflammatory process. In this article, we review the inflammatory role of microglia and astrocytes, focusing on their interactions with AD's core pathologies, amyloid beta deposition, and tau tangle formation. Additionally, we also discuss how different modes of regulated cell death in AD may impact the chronic neuroinflammatory environment. This review aims to highlight the evolving landscape of neuroinflammatory research in AD and underscores the importance of considering multiple cellular contributors when developing new therapeutic strategies.
引用
收藏
页数:21
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