Neurofilament light chain levels in neuronal surface antibody-associated autoimmune encephalitis: a systematic review and meta-analysis.

IF 5.8 1区医学 Q1 PSYCHIATRY

Translational Psychiatry Pub Date : 2025-01-25 DOI:10.1038/s41398-025-03241-6

Qi-Lun Lai, Meng-Ting Cai, Er-Chuang Li, Gao-Li Fang, Chun-Hong Shen, Yong-Feng Xu, Song Qiao, Jia-Jia Wang, Qin-Jie Weng, Yin-Xi Zhang

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引用次数: 0

Abstract

Background: Neuronal surface antibody-associated autoimmune encephalitis (NSAE) is a group of neuro-inflammatory disorders that is mediated by autoantibodies against the cell-surface and synaptic antigens. Studies have explored the role of neurofilament light chain (NfL) in NSAE and provided inconsistent data. We performed a systematic review and meta-analysis to evaluate the NfL levels in the serum and cerebrospinal fluid (CSF) of patients with NSAE.

Methods: The National Center for Biotechnology Information (NCBI, PubMed), Web of Knowledge, and the Cochrane Library databases were searched for studies reporting NfL levels in patients with NSAE. Random-effects meta-analysis was used to pool results across studies.

Results: Thirteen studies were included in the final systematic review and meta-analysis. The serum NfL levels were significantly higher in patients with NSAE compared to unaffected controls (standardized mean difference [SMD] = 0.909, 95% confidence interval [CI]: 0.536-1.282). Similarly, the CSF NfL levels were elevated in patients with NSAE (SMD = 0.897, 95% CI: 0.508-1.286). The serum and CSF NfL levels were not significantly correlated with disease severity, prognosis, and abnormalities in magnetic resonance imaging, electroencephalography, and CSF.

Conclusions: NfL levels in the serum and CSF were higher in patients with NSAE compared to unaffected controls. However, the NfL levels were not shown to be significantly associated with clinical or paraclinical features.

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来源期刊

Translational Psychiatry PSYCHIATRY-

CiteScore

11.50

自引率

2.90%

发文量

484

审稿时长

23 weeks

期刊介绍： Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.