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神经黏连蛋白-1 在神经退行性疾病的大脑和脑脊液中的研究:突触生物标志物的探索。

Neuroligin-1 in brain and CSF of neurodegenerative disorders: investigation for synaptic biomarkers.

机构信息

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden.

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.

出版信息

Acta Neuropathol Commun. 2021 Feb 1;9(1):19. doi: 10.1186/s40478-021-01119-4.

Abstract

Synaptic pathology is a central event in Alzheimer's disease (AD) and other neurodegenerative conditions, and investigation of synaptic proteins can provide valuable tools to follow synaptic dysfunction and loss in these diseases. Neuroligin-1 (Nlgn1) is a postsynaptic cell adhesion protein, important for synapse stabilization and formation. Nlgn1 has been connected to cognitive disorders, and specifically to AD, as target of the synaptotoxic effect of amyloid-β (Aβ) oligomers and Aβ fibrils. To address changes in Nlgn1 expression in human brain, brain regions in different neurological disorders were examined by Western blot and mass spectrometry. Brain specimens from AD (n = 23), progressive supranuclear palsy (PSP, n = 11), corticobasal degeneration (CBD, n = 10), and Pick's disease (PiD, n = 9) were included. Additionally, cerebrospinal fluid (CSF) samples of AD patients (n = 43) and non-demented controls (n = 42) were analysed. We found decreased levels of Nlgn1 in temporal and parietal cortex (~ 50-60% reductions) in AD brains compared with controls. In frontal grey matter the reduction was not seen for AD patients; however, in the same region, marked reduction was found for PiD (~ 77%), CBD (~ 66%) and to a lesser extent for PSP (~ 43%), which could clearly separate these tauopathies from controls. The Nlgn1 level was reduced in CSF from AD patients compared to controls, but with considerable overlap. The dramatic reduction of Nlgn1 seen in the brain extracts of tauopathies warrants further investigation regarding the potential use of Nlgn1 as a biomarker for these neurodegenerative diseases.

摘要

突触病理学是阿尔茨海默病(AD)和其他神经退行性疾病的核心事件,研究突触蛋白可以为这些疾病中突触功能障碍和丧失提供有价值的工具。神经黏附素 1(Nlgn1)是一种突触后细胞黏附蛋白,对于突触稳定和形成很重要。Nlgn1 与认知障碍有关,特别是与 AD 有关,它是淀粉样β(Aβ)寡聚体和 Aβ纤维的突触毒性作用的靶点。为了研究 Nlgn1 在人脑中的表达变化,通过 Western blot 和质谱法检查了不同神经退行性疾病的脑区。AD(n=23)、进行性核上性麻痹(PSP,n=11)、皮质基底节变性(CBD,n=10)和皮克病(PiD,n=9)的脑标本均包括在内。此外,还分析了 AD 患者(n=43)和非痴呆对照(n=42)的脑脊液(CSF)样本。我们发现 AD 大脑中的颞叶和顶叶皮质中的 Nlgn1 水平降低(约 50-60%减少),与对照组相比。在额叶灰质中,AD 患者未见减少;然而,在同一区域,PiD(77%)、CBD(66%)和 PSP(~43%)的减少明显,这可以清楚地将这些tau 病与对照组区分开来。与对照组相比,AD 患者的 CSF 中的 Nlgn1 水平降低,但重叠度较大。tau 病患者的脑提取物中 Nlgn1 的显著减少值得进一步研究,以确定 Nlgn1 是否可作为这些神经退行性疾病的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5be/7852195/a146c1299420/40478_2021_1119_Fig1_HTML.jpg

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