Small molecules to prevent the neurodegeneration caused by α-synuclein aggregation
Samuel Pe?a-Díaz1
Jordi Pujols1
Salvador Ventura2
1.Institut de Biotecnologia i Biomedicina,Departament de Bioquímica i Biologia Molecular,Universitat Autònoma de Barcelona,Bellaterra,Spain2.Institut de Biotecnologia i Biomedicina,Departament de Bioquímica i Biologia Molecular,Universitat Autònoma de Barcelona,Bellaterra,Spain;Institució Catalana de Recerca i Estudis Avan?ats(ICREA),Barcelona,Spain
摘要：Parkinson's disease (PD) is a neurodegenerative disorder belonging to a group of human pathologies known as synucleinopathies, which includes multiple system atrophy or dementia with Lewy bodies (Spill-antini et al., 1998). These diseases share a common neuropathological feature, the presence of α-synuclein (α-Syn) deposits, although they differ in the cellular and anatomical compartment in which α-Syn in-clusions accumulate. PD affects more than 1％ of people over 60 years of age, thus being the second most prevalent neurodegenerative disease in the world and the most common synucleinopathy. The loss of do-paminergic neurons in the substantia nigra pars compacta during PD progression induces a pronounced dopamine concentration decrease in the synaptic area, which translates into motor symptoms such as bradykinesia, rigidity or resting tremor (Martí et al., 2003). Damaged neurons were reported to have large proteinaceous inclusions, named Lewy's bodies and neurites, which constitute the major histopathologi-cal hallmark in PD. Amyloid fibrils of α-Syn were identified as the main component of these inclusions (Spillantini et al., 1997). The detection of genetic mutations (Polymeropoulos et al., 1997) and multiplications in the SNCA gene (Singleton et al., 2003), which encodes for α-Syn, linked to the early onset and higher penetrance of PD, provide evidence for the connection between the aggregation of this particular protein and PD.
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论文发表日期：2020-12-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 2260-2261 )