Multisensory gamma stimulation mitigates the effects of demyelination induced by cuprizone in male mice
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ABSTRACT:
PROVIDER: PRJNA1005296 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25635581_1.fastq.gz | Fastqsanger.gz | |||
| SRR25635581_2.fastq.gz | Fastqsanger.gz | |||
| SRR25635582_1.fastq.gz | Fastqsanger.gz | |||
| SRR25635582_2.fastq.gz | Fastqsanger.gz | |||
| SRR25635583_1.fastq.gz | Fastqsanger.gz |
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Project description:Demyelination is characterized by the loss of the myelin sheath that surrounds nerve fibers and myelin-supporting cells in the nervous system. This leads to increased vulnerability of axons to damage, resulting in significant atrophy and neuro-axonal degeneration. Demyelination is a common pathological feature in a wide range of diseases of the central nervous system (CNS). Multiple pathomolecular processes contribute to brain damage, including demyelination, neuroinflammation, oligodendrocyte (OLs) cell death, and progressive neuronal dysfunction. In this study, we used the cuprizone (CPZ) mouse model to investigate long-term non-invasive gamma entrainment using sensory stimulation (GENUS) as a potential therapeutic intervention for promoting myelination and reducing neuroinflammation. Our results demonstrate that GENUS effectively mitigated demyelination, stimulated oligodendrogenesis in the corpus callosum (CC), and preserved functional integrity and synaptic plasticity. Additionally, GENUS attenuated OLs ferroptosis-induced cell death. Furthermore, chronic GENUS exhibited a marked reduction in brain inflammation, decreasing both microgliosis and astrogliosis and proinflammatory molecules, such as high mobility group box 1 (HMGB1), complement component 1q (C1q) and complement C3 (C3). Considering the pro-remyelination and anti-neuroinflammatory effects observed with GENUS, these findings suggest its potential as a therapeutic approach for demyelinating disorders.
2024-06-07 | GSE240815 | GEO
Project description:We examined the role of TREM2 on microglia responses to demyelination Microglia were FACS-purified from WT or Trem2-/- mice fed with 0.2% cuprizone diet.
2015-04-22 | E-GEOD-66926 | biostudies-arrayexpress
Project description:Myelin abnormalities, oligodendrocyte damage, and concomitant glia activation are common in demyelinating diseases of the central nervous system (CNS). The neurotoxicant cuprizone (CPZ) has been extensively used to create a mouse model of demyelination. However, the changes of miRNA expression and effects on behavior of cuprizone treatment have not been clearly reported. We have analyzed the behavioral changes of mice given a diet containing 0.2% cuprizone for 6 weeks. To evaluate the changes of gene expression in CPZ-induced demyelination compared with control, we performed the GeneChip® mouse Gene 2.0 ST Array.
2019-03-30 | GSE129049 | GEO
Project description:Demyelination is a central pathological feature of multiple sclerosis and many other neurodegenerative diseases, and the cuprizone diet is a widely used model for studying this process. This study examines the transcriptional changes in key glial cell types—oligodendrocyte and astrocytes—during demyelination induced by a 4-week cuprizone diet. Bulk RNA sequencing was performed on these cells isolated using magnetic-activated cell sorting (MACS) from mice on either a normal diet or a 0.3% cuprizone diet. The experimental groups included: (1) oligodendrocytes and astrocytes from mice on a normal diet, and (2) oligodendrocytes and astrocytes from mice on a cuprizone diet. This study provides a comprehensive transcriptomic view of how these glial cell types respond to demyelination and will enhance our understanding of their individual and collective roles in this pathological process.
2025-08-17 | GSE287320 | GEO
Project description:Myelin abnormalities, oligodendrocyte damage, and concomitant glia activation are common in demyelinating diseases of the central nervous system (CNS). The neurotoxicant cuprizone (CPZ) has been extensively used to create a mouse model of demyelination. However, the changes of miRNA expression and effects on behavior of cuprizone treatment have not been clearly reported. We have analyzed the behavioral changes of mice given a diet containing 0.2% cuprizone for 6 weeks. To evaluate the changes of miRNA expression in CPZ-induced demyelination compared with control, we performed the Affymetrix GeneChip® miRNA 4.0 Array. We identified 1348 and 1253 differentially expressed miRNAs for control and CPZ-treated mice, respectively. Furthermore, the expression of 240 miRNAs was significantly changed in CPZ-induced mice comparing with control mice. These results suggest that the changes of miRNA expression in vivo may provide a new potential remyelination therapeutic target.
2018-11-22 | GSE122839 | GEO
Project description:Demyelination is a common pathological feature in a wide range of diseases, characterized by the loss of myelin sheath and myelin-supporting oligodendrocytes. These losses lead to impaired axonal function, increased vulnerability of axons to damage, and result in significant brain atrophy and neuro-axonal degeneration. Multiple pathomolecular processes contribute to neuroinflammation, oligodendrocyte cell death, and progressive neuronal dysfunction. In this study, we use the cuprizone mouse model of demyelination to investigate long-term non-invasive gamma entrainment using sensory stimulation as a potential therapeutic intervention for promoting myelination and reducing neuroinflammation in male mice. Here, we show that multisensory gamma stimulation mitigates demyelination, promotes oligodendrogenesis, preserves functional integrity and synaptic plasticity, attenuates oligodendrocyte ferroptosis-induced cell death, and reduces brain inflammation. Thus, the protective effects of multisensory gamma stimulation on myelin and anti-neuroinflammatory properties support its potential as a therapeutic approach for demyelinating disorders.
| S-EPMC11306744 | biostudies-literature
Project description:Demyelination and dysregulated myelination in the CNS are hallmarks of many neurodegenerative diseases such as multiple sclerosis (MS) and leukodystrophies. Here, we studied GFAP+ astrocytes during de- and remyelination in the cuprizone mouse by exploiting the ribosomal tagging (RiboTag) technology. Analyses were performed 5 weeks after cuprizone feeding, at the peak of demyelination in the corpus callosum, and 0.5 and 2 weeks after cuprizone withdrawal, when remyelination and tissue repair is initiated. After 5 weeks of cuprizone feeding, reactive astrocytes showed inflammatory signatures with enhanced expression of genes that modulate leukocyte migration (Tlr2, Cd86, Parp14,Cxcl10). Furthermore, demyelination-induced reactive astrocytes expressed numerous ligands including Cx3cl1, Csf1, Il34, and Gas6 that act on homeostatic as well as activated microglia and thus potentially mediate activation and recruitment of microglia as well as enhancement of their phagocytosis. During early remyelination, region-specific astrocytes displayed reduced inflammatory response signatures as indicated by shut down of CXCL10 production. During late remyelination, the signatures of GFAP+ astrocytes shifted towards resolving inflammation by active suppression of lymphocyte activation and differentiation and support of glia cell differentiation. Astrocytes showed enhanced expression of osteopontin (SPP1) as well as of factors that are relevant for tissue remodelling (Timp1), regeneration and axonal repair. In conclusion, we detected highly dynamic astroglial transcriptomic signatures in the cuprizone model, which reflects excessive communication amongst glia cells and highlights different astrocyte functions during neurodegeneration and regeneration.
2023-07-11 | GSE236805 | GEO
Project description:Demyelination and dysregulated myelination in the CNS are hallmarks of many neurodegenerative diseases such as multiple sclerosis (MS) and leukodystrophies. Here, we studied GFAP+ astrocytes during de- and remyelination in the cuprizone mouse by exploiting the ribosomal tagging (RiboTag) technology. Analyses were performed 5 weeks after cuprizone feeding, at the peak of demyelination in the corpus callosum, and 0.5 and 2 weeks after cuprizone withdrawal, when remyelination and tissue repair is initiated. After 5 weeks of cuprizone feeding, reactive astrocytes showed inflammatory signatures with enhanced expression of genes that modulate leukocyte migration (Tlr2, Cd86, Parp14,Cxcl10). Furthermore, demyelination-induced reactive astrocytes expressed numerous ligands including Cx3cl1, Csf1, Il34, and Gas6 that act on homeostatic as well as activated microglia and thus potentially mediate activation and recruitment of microglia as well as enhancement of their phagocytosis. During early remyelination, region-specific astrocytes displayed reduced inflammatory response signatures as indicated by shut down of CXCL10 production. During late remyelination, the signatures of GFAP+ astrocytes shifted towards resolving inflammation by active suppression of lymphocyte activation and differentiation and support of glia cell differentiation. Astrocytes showed enhanced expression of osteopontin (SPP1) as well as of factors that are relevant for tissue remodelling (Timp1), regeneration and axonal repair. In conclusion, we detected highly dynamic astroglial transcriptomic signatures in the cuprizone model, which reflects excessive communication amongst glia cells and highlights different astrocyte functions during neurodegeneration and regeneration.
2023-07-11 | GSE233951 | GEO
Project description:MicroRNA expression in the cuprizone-induced demyelination mouse model
| PRJNA506487 | ENA
Project description:Gene expression profile in the cuprizone-induced demyelination mouse model
| PRJNA529872 | ENA