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在食蟹猕猴灵长类动物中,α-突触核蛋白的年龄依赖性聚集。

Age-dependent α-synuclein aggregation in the Microcebus murinus lemur primate.

机构信息

Univ. de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, F-33000 Bordeaux, France.

出版信息

Sci Rep. 2012;2:910. doi: 10.1038/srep00910. Epub 2012 Nov 30.

DOI:10.1038/srep00910
PMID:23205271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3510464/
Abstract

Since age-dependent deposition of Aβ-amyloid has been reported in the Microcebusmurinus, we posited that this animal could as well be a model of age-related synucleinopathy. We characterized the distribution of Aβ-amyloid, α-synuclein and two of its modified forms in the brain of Microcebusmurinus aged from 1.5 to 10 years. Intracytoplasmic α-synuclein aggregates were observed only in aged animals in different brain regions, which were also phospho-Ser129 and nitrated α-synuclein immunoreactive. Age-dependent α-synuclein aggregation occurs spontaneously in mouse lemur primates. Microcebus murinus may provide a model to study age-associated α-synucleinopathy and for testing putative therapeutic interventions for both Alzheimer's and Parkinson's diseases.

摘要

由于在 Microcebusmurinus 中已经报道了与年龄相关的 Aβ-淀粉样蛋白沉积,我们假设这种动物也可能是与年龄相关的突触核蛋白病的模型。我们描述了 Aβ-淀粉样蛋白、α-突触核蛋白及其两种修饰形式在 1.5 至 10 岁 Microcebusmurinus 大脑中的分布。在不同的脑区,仅在老年动物中观察到细胞内α-突触核蛋白聚集物,这些聚集物还对磷酸化 Ser129 和硝化α-突触核蛋白呈免疫反应性。年龄依赖性α-突触核蛋白聚集在猕猴灵长类动物中自发发生。Microcebus murinus 可能为研究与年龄相关的α-突触核蛋白病以及测试针对阿尔茨海默病和帕金森病的潜在治疗干预措施提供模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6c6/3510464/83a1278dde8a/srep00910-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6c6/3510464/415e70a8be78/srep00910-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6c6/3510464/83a1278dde8a/srep00910-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6c6/3510464/415e70a8be78/srep00910-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6c6/3510464/83a1278dde8a/srep00910-f2.jpg

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