The Mechanisms of the Roles of α-Synuclein, Amyloid-β, and Tau Protein in the Lewy Body Diseases: Pathogenesis, Early Detection, and Therapeutics

被引：8

作者：

Noguchi-Shinohara, Moeko ^{[1
]}

Ono, Kenjiro ^{[1
]}

机构：

[1] Kanazawa Univ, Dept Neurol, Grad Sch Med Sci, Kanazawa 9208640, Japan

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2023年 / 24卷 / 12期

基金：

日本学术振兴会;

关键词：

alpha-synuclein; amyloid-beta; tau protein; aggregation; Lewy body diseases; Parkinson's disease; dementia with Lewy bodies; PHENOLIC-COMPOUNDS PREVENT; SLEEP BEHAVIOR DISORDER; PARKINSONS-DISEASE; CEREBROSPINAL-FLUID; MOUSE MODEL; ALZHEIMERS-DISEASE; MONOCLONAL-ANTIBODY; DEMENTIA; DIAGNOSIS; PROGRESSION;

D O I：

10.3390/ijms241210215

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：

Lewy body diseases (LBD) are pathologically defined as the accumulation of Lewy bodies composed of an aggregation of alpha-synuclein (aSyn). In LBD, not only the sole aggregation of alpha Syn but also the co-aggregation of amyloidogenic proteins, such as amyloid-beta (A beta) and tau, has been reported. In this review, the pathophysiology of co-aggregation of aSyn, A beta, and tau protein and the advancement in imaging and fluid biomarkers that can detect aSyn and co-occurring A beta and/or tau pathologies are discussed. Additionally, the alpha Syn-targeted disease-modifying therapies in clinical trials are summarized.

引用

页数：16

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