Exploring the intersection of atherosclerosis and Alzheimer's disease: the role of inflammation and complement activation

被引:0
作者
Vataja, Emilia [1 ]
Ratti, Giorgio [2 ]
Safa, Adrian [3 ]
Pagano, Marta [4 ]
Ferrante, Luigia [4 ]
Meri, Seppo [1 ,4 ,5 ]
Haapasalo, Karita [1 ]
机构
[1] Univ Helsinki, Dept Bacteriol & Immunol, Biomedicum 1 Haartmaninkatu 8, Helsinki 00014, Finland
[2] Univ Milan, Dept Pathophysiol & Transplantat, Via Francesco Sforza 35, I-20122 Milan, Italy
[3] Mayo Clin, Dept Neurol Surg, 4500 San Pablo Rd, Jacksonville, FL 32224 USA
[4] Humanitas Univ, Via R Levi Montalcini 4, I-20072 Milan, Italy
[5] Helsinki Univ Hosp, Diagnost Ctr, Topeliuksenkatu 32, Helsinki 00290, Finland
基金
芬兰科学院;
关键词
Complement; Inflammation; Neuroinflammation; Cardiovascular disease; FACTOR-H BINDS; APOLIPOPROTEIN-E; MOUSE MODELS; PROTEIN; SERUM; C1Q; C3; CHOLESTEROL; C5A; PATHWAY;
D O I
10.1007/s00011-025-02069-6
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
BackgroundAtherosclerosis (AS) and Alzheimer's disease (AD) are both multifactorial in nature and share many risk factors. Vascular dementia and AD may occur together, and a substantial proportion of AD cases also have signs of cardiovascular disease, a relationship well-established by cohort studies. The risk factors could contribute to persistent smoldering inflammation, including activation of complement at sites of endothelial injury and/or by accumulation of molecular aggregates.MethodsTo examine the possible bridging points between AD and AS, we constructed a comprehensive narrative review.ResultsA connecting point between AD and AS is inflammation. Contrary to prior assumptions, a significant linkage exists between systemic inflammation and neuroinflammation. Activities of complement, a key effector of innate immunity, are of special interest in the pathogenesis of both diseases.ConclusionAS and AD share a partially overlapping array of pathophysiological mechanisms.
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页数:13
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