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阿尔茨海默病、神经退行性变和神经炎症中的脑脊液神经鞘磷脂。

Cerebrospinal Fluid Sphingomyelins in Alzheimer's Disease, Neurodegeneration, and Neuroinflammation.

机构信息

Department of Population Health Sciences, University of Wisconsin-Madison, Madison, WI, USA.

Department of Genetics, School of Medicine, Stanford University, Stanford, CA, USA.

出版信息

J Alzheimers Dis. 2022;90(2):667-680. doi: 10.3233/JAD-220349.

DOI:10.3233/JAD-220349
PMID:36155504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9809197/
Abstract

BACKGROUND

Sphingomyelin (SM) levels have been associated with Alzheimer's disease (AD), but the association direction has been inconsistent and research on cerebrospinal fluid (CSF) SMs has been limited by sample size, breadth of SMs examined, and diversity of biomarkers available.

OBJECTIVE

Here, we seek to build on our understanding of the role of SM metabolites in AD by studying a broad range of CSF SMs and biomarkers of AD, neurodegeneration, and neuroinflammation.

METHODS

Leveraging two longitudinal AD cohorts with metabolome-wide CSF metabolomics data (n = 502), we analyzed the relationship between the levels of 12 CSF SMs, and AD diagnosis and biomarkers of pathology, neurodegeneration, and neuroinflammation using logistic, linear, and linear mixed effects models.

RESULTS

No SMs were significantly associated with AD diagnosis, mild cognitive impairment, or amyloid biomarkers. Phosphorylated tau, neurofilament light, α-synuclein, neurogranin, soluble triggering receptor expressed on myeloid cells 2, and chitinase-3-like-protein 1 were each significantly, positively associated with at least 5 of the SMs.

CONCLUSION

The associations between SMs and biomarkers of neurodegeneration and neuroinflammation, but not biomarkers of amyloid or diagnosis of AD, point to SMs as potential biomarkers for neurodegeneration and neuroinflammation that may not be AD-specific.

摘要

背景

神经鞘磷脂 (SM) 水平与阿尔茨海默病 (AD) 有关，但关联方向一直不一致，而且脑脊液 (CSF) SM 的研究受到样本量、检查的 SM 广度和可用生物标志物多样性的限制。

目的

在这里，我们通过研究广泛的 CSF SM 和 AD、神经退行性变和神经炎症的生物标志物，旨在进一步了解 SM 代谢物在 AD 中的作用。

方法

利用具有代谢组学 CSF 代谢组学数据的两个纵向 AD 队列（n = 502），我们使用逻辑、线性和线性混合效应模型分析了 12 种 CSF SM 水平与 AD 诊断以及病理、神经退行性变和神经炎症的生物标志物之间的关系。

结果

没有 SM 与 AD 诊断、轻度认知障碍或淀粉样生物标志物显著相关。磷酸化 tau、神经丝轻链、α-突触核蛋白、神经颗粒蛋白、髓样细胞触发受体 2 可溶性、几丁质酶 3 样蛋白 1 均与至少 5 种 SM 呈显著正相关。

结论

SM 与神经退行性变和神经炎症的生物标志物之间的关联，而不是淀粉样生物标志物或 AD 诊断，表明 SM 可能是神经退行性变和神经炎症的潜在生物标志物，而不是 AD 特异性的生物标志物。