Targeting transglutaminase 2 as a potential disease modifying therapeutic strategy for synucleinopathies  

作　　者：Jie Zhang Hilary Grosso Jasutkar M.Maral Mouradian 

机构地区：[1]Robert Wood Johnson Medical School Institute for Neurological Therapeutics,and Department of Neurology,Rutgers Biomedical and Health Sciences,Piscataway,NJ,USA

出　　处：《Neural Regeneration Research》2021年第8期1560-1561,共2页中国神经再生研究（英文版）

基　　金：supported by grants from the Michael J. Fox Foundation for Parkinson’s Research (ID 12350);the American Parkinson Disease Association, the New Jersey Health Foundation, and by NIH grants NS101134, NS096032, and NS116921。

摘　　要：Synucleinopathies are a group of progressive neurodegenerative disorders characterized by the accumulation of α-synuclein(α-Syn) aggregates in Lewy bodies(LBs) and Lewy neurites(LNs) in Parkinson's disease(PD) and dementia with Lewy bodies(DLB), and in glial cytoplasmic inclusions in multiple system atrophy(MSA). α-Syn is a 140 amino acid intrinsically disordered protein, which tends to self-aggregate and form fibrils in these neuropathological hallmark inclusions. Several lines of evidence sug gest that misfolding and aggregation of α-Syn is a critical step leading to neuronal dysfunction and death.

关 键 词：ATROPHY THERAPEUTIC AGGREGATION 

分 类 号：R741[医药卫生—神经病学与精神病学]