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超越α-突触核蛋白转移:帕金森病中的病理学传播。

Beyond α-synuclein transfer: pathology propagation in Parkinson's disease.

机构信息

Neural Plasticity and Repair Unit, Wallenberg Neuroscience Center, Lund University, BMC A10 22184, Lund, Sweden.

出版信息

Trends Mol Med. 2012 May;18(5):248-55. doi: 10.1016/j.molmed.2012.03.002. Epub 2012 Apr 13.

Abstract

α-Synuclein (α-syn) is the most abundant protein found in Lewy bodies, a hallmark of Parkinson's disease (PD), and can aggregate to form toxic oligomers and fibrillar structures. Recent studies have shown that α-syn can be transmitted between neurons and can seed the formation of toxic aggregates in recipient neurons in a prion-like manner. In addition, it is known that Lewy body pathology may spread gradually and systematically from the peripheral or enteric nervous system or olfactory bulb to specific brain regions during progression of idiopathic PD. It is therefore conceivable that α-syn species could act as seeds that drive PD progression. Here, we review recent advances from studies of α-syn cell-to-cell transfer, the current understanding of α-syn toxicity, and how these relate to progression of PD pathology.

摘要

α-突触核蛋白(α-syn)是路易小体中含量最丰富的蛋白质,路易小体是帕金森病(PD)的标志,可聚集形成毒性寡聚物和纤维状结构。最近的研究表明,α-syn 可以在神经元之间传递,并以类朊病毒的方式在受体内诱导形成毒性聚集物。此外,已知路易小体病理学可能在特发性 PD 进展过程中逐渐和系统地从周围或肠神经系统或嗅球传播到特定脑区。因此,可以想象 α-syn 种可能作为驱动 PD 进展的种子。在这里,我们回顾了最近关于 α-syn 细胞间转移的研究进展,以及目前对 α-syn 毒性的理解,以及这些如何与 PD 病理进展相关。

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