Results 51 to 60 of about 6,317 (193)

Cerebellar Cortical Demyelination in the Murine Cuprizone Model

open access: yesBrain Pathology, 2010
AbstractIn multiple sclerosis, demyelination occurs beside the white‐matter structures and in the cerebral and cerebellar cortex. We have previously shown that, in the cuprizone model, demyelination is present not only in the corpus callosum but also in the cerebral cortex.
Thomas, Skripuletz   +7 more
openaire   +3 more sources

In Vivo Measurement of Neurochemical Abnormalities in the Hippocampus in a Rat Model of Cuprizone-Induced Demyelination

open access: yesDiagnostics, 2020
This study quantitatively measured the changes in metabolites in the hippocampal lesions of a rat model of cuprizone-induced demyelination as detected using in vivo 7 T proton magnetic resonance spectroscopy.
Do-Wan Lee   +7 more
doaj   +1 more source

Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance

open access: yesMolecular Neurodegeneration, 2022
Background Microglia regulate the response to injury and disease in the brain and spinal cord. In white matter diseases microglia may cause demyelination. However, how microglia respond and regulate demyelination is not fully understood.
Sameera Zia   +15 more
doaj   +1 more source

Effects of Tributyltin Chloride on Human Neuronal Differentiation and Mice Brain Development

open access: yesEnvironmental Toxicology, Volume 41, Issue 10, Page 906-921, October 2026.
ABSTRACT According to the developmental origins of health and disease hypothesis, perinatal exposure to an environmental toxicant during the development of the nervous system could cause a permanent cellular modification that may promote the appearance of neurodegenerative diseases at an older age.
Ester López‐Gallardo   +10 more
wiley   +1 more source

Spatio-Temporal Patterns of Demyelination and Remyelination in the Cuprizone Mouse Model. [PDF]

open access: yesPLoS ONE, 2016
Cuprizone administration in mice provides a reproducible model of demyelination and spontaneous remyelination, and has been useful in understanding important aspects of human disease, including multiple sclerosis.
Ian Tagge   +9 more
doaj   +1 more source

NG2‐Glia in Central Nervous System Following Injury: From Pathological Involvement to Repair Potential

open access: yesCNS Neuroscience &Therapeutics, Volume 32, Issue 9, September 2026.
Following CNS injury, NG2‐glia display distinct functional phases. In the early stage, NG2‐glia are rapidly activated, proliferate, migrate to the lesion site and secrete CSPGs, which form a chemical and physical barrier that inhibits axonal regeneration.
Yunyun Cai   +4 more
wiley   +1 more source

Microglia and neuroinflammation: An in‐depth analysis from functional diversity to disease mechanisms

open access: yesClinical and Translational Medicine, Volume 16, Issue 9, September 2026.
1. Microglial functions arise from dynamic, context‐dependent programs rather than fixed M1/M2 phenotypes. 2. Inflammatory, interferon‐responsive, phagocytic/lipid‐metabolic and repair‐associated programs coexist across disease stages and brain regions. 3.
Jie Chen   +6 more
wiley   +1 more source

Deep gray matter demyelination detected by magnetization transfer ratio in the cuprizone model. [PDF]

open access: yesPLoS ONE, 2013
In multiple sclerosis (MS), the correlation between lesion load on conventional magnetic resonance imaging (MRI) and clinical disability is weak. This clinico-radiological paradox might partly be due to the low sensitivity of conventional MRI to detect ...
Sveinung Fjær   +6 more
doaj   +1 more source

Tissue‐Resident Macrophage in Inflammation and Cancer

open access: yesMedComm, Volume 7, Issue 9, September 2026.
Opposing macrophage functions in inflammation and cancer converge on shared mechanistic nodes, informing cross‐disease therapeutic strategies. ABSTRACT Tissue‐resident macrophages (TRMs) are long‐lived immune cells strategically distributed across organs, where their functional plasticity enables both homeostatic maintenance and pathological ...
Siyuan Huang   +13 more
wiley   +1 more source

Leucine Supplementation in Cuprizone-Induced Oligodendrocyte Toxicity [PDF]

open access: yes, 2019
Cuprizone is a copper chelator that induces demyelination in the central nervous system when fed to mice. This compound is thought to target Complex IV and disrupt mitochondrial metabolism leading to loss of myelin-producing oligodendrocytes.
Ley, Michael
core  

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