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Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

ABSTRACT: Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

PROVIDER: PRJNA940750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23698535_1.fastq.gz	Fastqsanger.gz
	SRR23698535_2.fastq.gz	Fastqsanger.gz
	SRR23698536_1.fastq.gz	Fastqsanger.gz
	SRR23698536_2.fastq.gz	Fastqsanger.gz
	SRR23698537_1.fastq.gz	Fastqsanger.gz

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Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

Project description:Blood-based neurofilament light (sNfL) indicates neuroaxonal injury in multiple sclerosis and is on the cusp of being implemented into clinical routine. However, anatomical origins and pathophysiological mechanisms of NfL release during acute relapses and later chronic disease stages are still poorly understood. Here, we applied immunohistochemistry, single molecule array, spatial transcriptomics and microglia/axon co-cultures to gain insight into spatio-temporal NfL release in experimental autoimmune encephalomyelitis (EAE). Results: Association of spinal cord white matter lesions and sNfL levels revealed a distinct, stage-dependent anatomical pattern of neuroaxonal damage: In chronic EAE, sNfL levels were predominately associated with anterolateral lumbar lesions, whereas in early EAE sNfL showed no correlation with lesions in any anatomical location. Furthermore, neuroaxonal damage in late EAE was largely confined to white matter lesions, but showed a widespread distribution in early EAE. Followingthis spatio-temporal pattern of neuroaxonal damage, spatial transcriptomics revealed a widespread cyto- and chemokine response at early disease stages, whereas late EAE was characterized by a prominent glial cell accumulation in white matter lesions. These findings were corroborated by immunohistochemistry and micro-glia/axon co-cultures, which further revealed a strong association between CNS myeloid cell activation and neuroaxonal damage both in vivo and in vitro. Interpretation: Our data demonstrate that sNfL release in EAE driven by CNS myeloid cells exhibits progress in a disease stage-dependent centripetal manner from normal-appearing white matter to focal white matter lesions. These findings may further aid the interpretation of elevated sNfL levels in multiple sclerosis patients at different disease stages.

2023-11-22 | GSE226591 | GEO

Secreted neurofilament light chain (NfL) after neuronal damage induces myeloid cell activation and neuroinflammation [scRNA-Seq]

Project description:Secreted neurofilament light chain (NfL) after neuronal damage induces myeloid cell activation and neuroinflammation [scRNA-Seq]

| PRJNA1214588 | ENA

Secreted neurofilament light chain (NfL) after neuronal damage induces myeloid cell activation and neuroinflammation [bulkRNA-Seq]

Project description:Secreted neurofilament light chain (NfL) after neuronal damage induces myeloid cell activation and neuroinflammation [bulkRNA-Seq]

| PRJNA1214826 | ENA

Secreted neurofilament light chain (NfL) after neuronal damage induces myeloid cell activation and neuroinflammation [bulkRNA-Seq]

Project description:Neurofilament light chain (NfL) is a neuron-specific cytoskeletal protein that provides structural support for axons and is released into the extracellular space following neuronal injury. While NfL has been extensively studied as a disease biomarker, the underlying release mechanisms and role in neurodegeneration remain poorly understood. Here, we find that neurons secrete low baseline levels of NfL, while neuronal damage triggers calpain-driven proteolysis and release of fragmented NfL. Secreted NfL activates microglia cells, which can be blocked with anti-NfL antibodies. We utilize in vivo single-cell RNA sequencing to profile brain cells after injection of recombinant NfL into the mouse hippocampus and find robust macrophage and microglial responses. Consistently, NfL knock-out mice ameliorate microgliosis and delay symptom onset in the SOD1 mouse model of amyotrophic lateral sclerosis (ALS). Our results show that released NfL can activate myeloid cells in the brain and is, thus, a potential therapeutic target for neurodegenerative diseases.

2025-01-27 | GSE287862 | GEO

Secreted neurofilament light chain (NfL) after neuronal damage induces myeloid cell activation and neuroinflammation [scRNA-Seq]

2025-01-27 | GSE287769 | GEO

Gene expression changes in LPS-induced neuroinflammation

Project description:Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 ug) was administered into the lateral ventricle of mice and, 24 hours later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation. Mice were given intracerebroventricular injections of saline vehicle (n = 4) or lipopolysaccharide (n = 4). Twenty-four hours later, we dissected the hippocampus and cerebral cortex and processed the tissue for microarray analysis. Gene expression changes observed in the microaray data were validated with quantitative real-time PCR.

2008-11-01 | E-GEOD-12284 | biostudies-arrayexpress

Spatial transcriptomics and neurofilament light chain reveal changes in lesion patterns in murine autoimmune neuroinflammation.

Project description:ObjectiveOngoing neuroaxonal damage is a major contributor to disease progression and long-term disability in multiple sclerosis. However, spatio-temporal distribution and pathophysiological mechanisms of neuroaxonal damage during acute relapses and later chronic disease stages remain poorly understood.MethodsHere, we applied immunohistochemistry, single-molecule array, spatial transcriptomics, and microglia/axon co-cultures to gain insight into spatio-temporal neuroaxonal damage in experimental autoimmune encephalomyelitis (EAE).ResultsAssociation of spinal cord white matter lesions and blood-based neurofilament light (sNfL) levels revealed a distinct, stage-dependent anatomical pattern of neuroaxonal damage: in chronic EAE, sNfL levels were predominately associated with anterolateral lumbar lesions, whereas in early EAE sNfL showed no correlation with lesions in any anatomical location. Furthermore, neuroaxonal damage in late EAE was largely confined to white matter lesions but showed a widespread distribution in early EAE. Following this pattern of neuroaxonal damage, spatial transcriptomics revealed a widespread cyto- and chemokine response at early disease stages, whereas late EAE was characterized by a prominent glial cell accumulation in white matter lesions. These findings were corroborated by immunohistochemistry and microglia/axon co-cultures, which further revealed a strong association between CNS myeloid cell activation and neuroaxonal damage both in vivo and in vitro.InterpretationOur findings indicate that CNS myeloid cells may play a crucial role in driving neuroaxonal damage in EAE. Moreover, neuroaxonal damage can progress in a stage-dependent centripetal manner, transitioning from normal-appearing white matter to focal white matter lesions. These insights may contribute to a better understanding of neurodegeneration and elevated sNfL levels observed in multiple sclerosis patients at different disease stages.

| S-EPMC10644497 | biostudies-literature

Lesion Segregation

Project description:Liver Cancer Evolution - Lesion segregation

| PRJEB37808 | ENA

Vagus Nerve Stimulation enhances remyelination and decreases innate neuroinflammation in a Multiple Sclerosis rodent model.

Project description:This study investigated the effect of Vagus Nerve Stimulation (VNS) on innate neuroinflammation and remyelination in lysolecithin (LPC) induced demyelination, a preclinical model for Multiple Sclerosis (MS). In a first experiment (demyelination experiment), LPC was injected in the corpus callosum of 33 Lewis rats, inducing a demyelinated lesion, and rats were treated with either continuously-cycled VNS (cVNS) or one-minute per day VNS (1minVNS) or sham VNS, from two days before the injection until three days post-injection (dpi), when they were killed for immunohistochemistry and proteomics analysis. This timepoint corresponded with a demyelinated lesion and peak inflammation. In a second experiment (remyelination experiment), 13 rats were analogously treated with either cVNS or sham from two days before LPC injection until 11 dpi, when they were killed for tissue prelevation for immunohistochemistry and proteomics. This timepoints corresponded with partial remyelination of the lesion. For proteomics analysis, 20 rats were randomly selected, namely five cVNS and five sham rats of the demyelination experiment, and five cVNS and five sham rats of the remyelination experiment.

2024-05-10 | PXD050858 | Pride

Lesion-dependent Hdac8 interactome

Project description:In this project anti-Hdac8 immunoaffinity purifications (IPs) of nerves isolated from WT and Hdac8 knock out mice were compared. Nerves were either crushed prior IP (lesion, CR) or not (no lesion, CO). IPs were performed 1 dpL. In total four IPs were performed.

2024-12-02 | PXD046582 | Pride

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