Serum NfL associated with anti-NMDA receptor encephalitis

Ma, Xiaoyu; Lu, Yaxin; Peng, Fuhua; Wang, Yuge; Sun, Xiaobo; Luo, Wenjing; Shen, Shishi; Liu, Zifeng; Kermode, Allan G.; Qiu, Wei; Shu, Yaqing

doi:10.1007/s10072-021-05838-3

Cited by 7 publications

(12 citation statements)

References 13 publications

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“…However, compared to cognitively normal controls, NfL and YKL-40 were elevated in AE patients, indicating neuroaxonal damage and astroglial activation, respectively (Day et al 2021). The study confirms previous findings of elevated YKL-40 concentrations in CSF of NMDARE patients (Chen et al 2018) and is in line with another report showing increased serum NfL concentrations in NMDARE patients compared to healthy controls (Ma et al 2022). Neurogranin and SNAP-25 were decreased in CSF of AE patients suggesting synaptic dysfunction.…”

Section: Cerebrospinal Fluid Parameterssupporting

confidence: 93%

“…Whereas neuronal loss was absent in tumor free frontal regions and the hippocampus despite the presence of perivascular CD79a+ B cells (Mariotto et al 2019) suggesting that the presence of neuronal damage may depend on underlying or concomitant pathologies. Indirect evidence for CNS injury, neuronal and neuroaxonal damage was obtained in three studies that found elevated serum concentrations of neurofilament light chain, neuron specific enolase, and S100b in NMDARE patients (Liu et al 2018b, Guasp et al 2022, Ma et al 2022). Hence, neuronal damage can be assumed in some NMDARE cases but does not seem to be a major determinant of NMDARE pathogenesis.…”

Section: Neuropathologymentioning

confidence: 99%

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Modeling anti-NMDAR encephalitis

Wilke¹

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ASC, antibody secreting cell BBB, blood-brain barrier CNP, 2'-3'-cylcic nucleotide 3'-phosphodiesterase CNS, central nervous system CSF, cerebrospinal fluid DTA, diphtheria toxin fragment A EEG, electroencephalography GABAAR, GABAA receptor GABABR, GABAB receptor HSE, herpes simplex encephalitis HSV, herpes simplex virus IgA, immunoglobulin A IgG, immunoglobulin G IgM, immunoglobulin M JE, Japanese encephalitis JEV, Japanese encephalitis virus KO, knockout LTP, long-term potentiation MRI, magnetic resonance imaging mRS, modified Rankin scale NMDA, N-methyl-D-aspartate NMDAR, NMDA receptor NMDARE, anti-NMDAR encephalitis OCB, oligoclonal bands PET, positron emission tomography rs-fMRI, resting state functional MRI WBC, white blood cell count

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Section: Cerebrospinal Fluid Parameterssupporting

confidence: 93%

Section: Neuropathologymentioning

confidence: 99%

Modeling anti-NMDAR encephalitis

Wilke¹

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“…In two studies including both NSA-AEs and other AEs, initial CSF levels of NFL, but not of T-tau, correlated with disability (expressed as score on the modified Rankin Scale, mRS) at last follow-up (namely, after 12 months) [ 135 , 136 ]. Similar findings were confirmed for NMDAR and LGI1 encephalitides [ 142 , 148 ], although not in all cohorts [ 138 , 140 ], as well as for serum NFL in NMDAR encephalitis, with the biomarker discriminating between patients with mRS score above vs. below 2 at 1-year follow-up with an area under the curve (AUC) of 0.697 [ 141 ]. In agreement with this, serum NFL is lower in NMDAR encephalitis patients with good treatment response compared to those with poor response [ 141 ].…”

Section: Secondary Neurodegeneration In Patients With Autoimmune Ence...mentioning

confidence: 52%

Neural Surface Antibodies and Neurodegeneration: Clinical Commonalities and Pathophysiological Relationships

et al. 2023

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Autoimmune encephalitis and neurodegenerative disorders share several clinical features, including behavioural and psychiatric manifestations, cognitive impairment, sleep and movement disorders. Therefore, it is not surprising that autoimmune encephalitis is one of the main differential diagnoses of rapidly progressive dementia. However, more chronic presentations of autoimmune disorders have been reported and can lead to the misdiagnosis of a neurodegenerative disease. On the other hand, antibodies against neuronal proteins, such as those directed against NMDAR, can occur during established neurogenerative disorders, and their role in this context is still unclear. They might be simple bystanders or modify the disease course and phenotype. Indeed, autoimmune encephalitis can leave long-term cognitive sequelae and specific antibodies to neuronal surface antigens are associated with clinical and pathological neurodegenerative features. Here we review the link between these antibodies and neurodegeneration. In particular we discuss: (a) the possibility that autoimmune encephalitis presents as a neurodegenerative disease, identifying the red flags that can help in the differential diagnosis between antibody-mediated and neurodegenerative disorders; (b) the occurrence of antibodies against neuronal surface antigens in patients with neurodegenerative disorders and their possible role in the disease course; and (c) the long-term cognitive and neuroradiological changes associated with autoimmune encephalitis, as well as the biomarkers that can help to predict the cognitive outcome. Finally, we review the clinical and pathological features of IgLON5 antibodies-related encephalitis, a unique model of the relationship between antibodies and neurodegeneration.

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“…Notably, the enhanced thalamocortical connectivity was positively correlated with convalescent sNfL levels in the patient cohort. As mentioned above, sNfL levels were clinically associated with the disease severity and functional status of anti‐NMDAR encephalitis (Ma et al, 2022b; Macher et al, 2021). Furthermore, sNfL, a biomarker of neuroaxonal injury, has been found to be linked with persistent neuroinflammation and neurodegeneration (Srpova et al, 2021).…”

Section: Discussionmentioning

confidence: 91%

Serum neurofilament light chain is associated with disturbed limbic‐based functional connectivity in patients with anti‐NMDAR encephalitis

Chen

Fang

Peng

et al. 2022

Journal of Neurochemistry

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Anti-N-methyld-aspartate receptor (NMDAR) encephalitis shows a predilection for affecting the limbic system, but structural MRI in most patients is usually unremarkable. However, the functional connectivity reorganization of limbic nodes remains unknown. Serum neurofilament light chains (sNfL) are clinically linked with the disease severity and neurological disability of anti-NMDAR encephalitis. However, the relationship between sNfL and limbic-based functional architecture has not been explored. We consecutively recruited 20 convalescent patients with anti-NMDAR encephalitis and 24 healthy controls from March 2018 to March 2021. Resting-state functional MRI metrics, including fractional amplitude of low-frequency fluctuation (fALFF), regional homogeneity (ReHo), and atlas-based seed functional connectivity, were analyzed to investigate regional activities and functional connectivity alterations. Correlation analysis among functional connectivity, sNfL, Mini-Mental State Examination (MMSE), and Montreal cognitive assessment outcomes were explored in patients. Compared with those of healthy controls, the fALFF and ReHo were consistently increased in regions of the posterior default mode network (DMN) hub, mainly the bilateral supramarginal gyrus and precuneus, in patients with anti-NMDAR encephalitis (FWE-corrected p < 0.05). Patients demonstrated disturbed functional organization characterized by reduced connectivity of the posterior DMN hub with the sensorimotor cortex and hypoconnectivity of the parahippocampal gyrus (PHG) with the right fusiform gyrus but extensively enhanced thalamocortical connectivity (FWE-corrected p < 0.05). Furthermore, convalescent sNfL showed a positive correlation with enhanced thalamocortical connectivity (r = 0.4659, p = 0.0384). Onset sNfL with an independent linear correlation to convalescent MMSE performance (B coefficient, −0.013, 95% CI, −0.025 ~ −0.002, p = 0.0260) was positively correlated with intra-DMN connectivity (r = 0.8969, p < 0.0001) and limbic-sensory connectivity (r = 0.4866, p = 0.0346 for hippocampus seed and r = 0.5218, p = 0.0220 for PHG | 211 CHEN et al.

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Serum NfL associated with anti-NMDA receptor encephalitis

Cited by 7 publications

References 13 publications

Modeling anti-NMDAR encephalitis

Modeling anti-NMDAR encephalitis

Neural Surface Antibodies and Neurodegeneration: Clinical Commonalities and Pathophysiological Relationships

Serum neurofilament light chain is associated with disturbed limbic‐based functional connectivity in patients with anti‐NMDAR encephalitis

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