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Updated: Jul 8, 2026

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis
Published on: February 23, 2024
[Neurofilament protein light in multiple sclerosis]
Yan Zhang1, Xiang Li, Jian Qiao
1Institute of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Objective:
To determine if neurofilament protein light (NF-L) and anti-NF-L antibody can be used as biologic markers in diagnosing multiple sclerosis (MS) and assessing prognosis thereof.
Methods:
Samples of cerebrospinal fluid (CSF) and serum were corrected from 63 MS patients, 15 patients with neuromyelitis optica (ONM), 31 patients with other inflammatory neurological disease (OIND), 18 patients with noninflammatory neurological disease (NIND), and 46 neurological normal controls (NC group), all age- and sex- matched. ELISA was used to detect the concentrations of NF-L, anti-NF-L antibody, anti-myelin basic protein (MBP) antibody, and anti-myelin oligo-dendroglia glycoprotein (MOG) antibody in serum and cerebral spinal fluid. And the IgG level was tested.
Results:
The CSF levels of NF-L of the MS, ONM, OIND, and NIND groups were 26 ng/L (33), 20 ng/L (92), 19 ng/L (82), and 30 ng/L (194) respectively, without significant differences among these different groups, but all significantly higher than that of the NC group (10 ng/L, all P < 0.01). No NF-L was detected in the serum specimens of all groups. The CSF NF-L antibody level of the MS group was significantly lower than that of the OIND group (P < 0.01), and significantly higher than those of the NIND and NC groups (both P < 0.05). The CSF anti-NF-L antibody level of the MS patients was positively correlated with the MBP antibody level (r = 0.784, P < 0.01) and the IgG level (r = 0.675, P < 0.01).
Conclusion:
Neither the NF-L nor the anti-NF-L antibody can be used as reliable biological markers for the diagnosis of MS. Strongly increased levels of NF-L were observed in patients with MS, ONM, OIND, and NIND, suggesting the occurrence of axonal injury in these conditions. Inflammation may not lead to the generation of anti-NF-L antibody which links to the axonal injury.
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