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阿尔茨海默病中的细胞焦亡:小胶质细胞、星形胶质细胞和神经元中的细胞类型特异性激活

Pyroptosis in Alzheimer's disease: cell type-specific activation in microglia, astrocytes and neurons.

作者信息

Moonen Sebastiaan, Koper Marta J, Van Schoor Evelien, Schaeverbeke Jolien M, Vandenberghe Rik, von Arnim Christine A F, Tousseyn Thomas, De Strooper Bart, Thal Dietmar Rudolf

机构信息

Laboratory for Neuropathology, Department of Imaging and Pathology, Leuven Brain Institute (LBI), KU Leuven (University of Leuven), O&N IV Herestraat 49, Bus 1032, 3000, Leuven, Belgium.

Laboratory for the Research of Neurodegenerative Diseases, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven (University of Leuven), Leuven, Belgium.

出版信息

Acta Neuropathol. 2023 Feb;145(2):175-195. doi: 10.1007/s00401-022-02528-y. Epub 2022 Dec 9.

Abstract

The major neuropathological hallmarks of Alzheimer's disease (AD) are amyloid β (Aβ) plaques and neurofibrillary tangles (NFT), accompanied by neuroinflammation and neuronal loss. Increasing evidence is emerging for the activation of the canonical NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome in AD. However, the mechanisms leading to neuronal loss in AD and the involvement of glial cells in these processes are still not clear. The aim of this study was to investigate the contribution of pyroptosis, a pro-inflammatory mechanism of cell death downstream of the inflammasome, to neurodegeneration in AD. Immunohistochemistry and biochemical analysis of protein levels were performed on human post-mortem brain tissue. We investigated the presence of cleaved gasdermin D (GSDMD), the pyroptosis effector protein, as well as the NLRP3 inflammasome-forming proteins, in the medial temporal lobe of 23 symptomatic AD, 25 pathologically defined preclinical AD (p-preAD) and 21 non-demented control cases. Cleaved GSDMD was detected in microglia, but also in astrocytes and in few pyramidal neurons in the first sector of the cornu ammonis (CA1) of the hippocampus and the temporal cortex of Brodmann area 36. Only microglia expressed all NLRP3 inflammasome-forming proteins (i.e., ASC, NLRP3, caspase-1). Cleaved GSDMD-positive astrocytes and neurons exhibited caspase-8 and non-canonical inflammasome protein caspase-4, respectively, potentially indicating alternative pathways for GSDMD cleavage. Brains of AD patients exhibited increased numbers of cleaved GSDMD-positive cells. Cleaved GSDMD-positive microglia and astrocytes were found in close proximity to Aβ plaques, while cleaved GSDMD-positive neurons were devoid of NFTs. In CA1, NLRP3-positive microglia and cleaved GSDMD-positive neurons were associated with local neuronal loss, indicating a possible contribution of NLRP3 inflammasome and pyroptosis activation to AD-related neurodegeneration. Taken together, our results suggest cell type-specific activation of pyroptosis in AD and extend the current knowledge about the contribution of neuroinflammation to the neurodegenerative process in AD via a direct link to neuron death by pyroptosis.

摘要

阿尔茨海默病(AD)的主要神经病理学特征是β-淀粉样蛋白(Aβ)斑块和神经原纤维缠结(NFT),同时伴有神经炎症和神经元丢失。越来越多的证据表明,AD中含核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体被激活。然而,导致AD中神经元丢失的机制以及神经胶质细胞在这些过程中的作用仍不清楚。本研究的目的是探讨炎性小体下游的一种促炎细胞死亡机制——细胞焦亡对AD神经退行性变的影响。对人类尸检脑组织进行了免疫组织化学和蛋白质水平的生化分析。我们研究了23例有症状的AD患者、25例病理诊断为临床前期AD(p-preAD)患者和21例非痴呆对照者的内侧颞叶中裂解的gasdermin D(GSDMD)(细胞焦亡效应蛋白)以及形成NLRP3炎性小体的蛋白的存在情况。在小胶质细胞中检测到了裂解的GSDMD,在星形胶质细胞以及海马齿状回(CA1)第一区和布罗德曼36区颞叶皮质的少数锥体神经元中也检测到了。只有小胶质细胞表达所有形成NLRP3炎性小体的蛋白(即凋亡相关斑点样蛋白(ASC)、NLRP3、半胱天冬酶-1)。裂解的GSDMD阳性星形胶质细胞和神经元分别表现出半胱天冬酶-8和非经典炎性小体蛋白半胱天冬酶-4,这可能表明GSDMD裂解的替代途径。AD患者的大脑中裂解的GSDMD阳性细胞数量增加。在靠近Aβ斑块处发现了裂解的GSDMD阳性小胶质细胞和星形胶质细胞,而裂解的GSDMD阳性神经元没有神经原纤维缠结。在CA1区,NLRP3阳性小胶质细胞和裂解的GSDMD阳性神经元与局部神经元丢失有关,这表明NLRP3炎性小体和细胞焦亡激活可能对AD相关的神经退行性变有影响。综上所述,我们的结果表明AD中细胞焦亡存在细胞类型特异性激活,并通过与细胞焦亡导致的神经元死亡的直接联系,扩展了目前关于神经炎症对AD神经退行性变过程影响的认识。

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