ArticleFrontiers in aging neuroscience2018
Age Influences Microglial Activation After Cuprizone-Induced Demyelination.
Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Therapeutic potential and underlying mechanisms of engineered young plasma-derived exosomes in Alzheimer's disease.Bioactive materials · 2027Article
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- PAC1 Receptor Knockout Mice Reveal Critical Links Between ER Stress, Myelin Homeostasis, and Neurodegeneration.International journal of molecular sciences · 2025Article
- PET imaging of neuroinflammation: any credible alternatives to TSPO yet?Molecular psychiatry · 2025Review
- Implications of disease-modifying therapies for multiple sclerosis on immune cells and response to COVID-19 vaccination.Frontiers in immunology · 2024Article
- Diagnostic efficacy of long non-coding RNAs in multiple sclerosis: a systematic review and meta-analysis.Frontiers in genetics · 2024Review
- Cu,Zn-Superoxide Dismutase has Minimal Effects Against Cuprizone-Induced Demyelination, Microglial Activation, and Neurogenesis Defects in the C57BL/6 Mouse Hippocampus.Neurochemical research · 2023Article
- Fractalkine enhances oligodendrocyte regeneration and remyelination in a demyelination mouse model.Stem cell reports · 2023Article
- Immunosenescence and multiple sclerosis: inflammaging for prognosis and therapeutic consideration.Frontiers in aging · 2023Review
- Article
- Comparison of the Effects of Cuprizone on Demyelination in the Corpus Callosum and Hippocampal Progenitors in Young Adult and Aged Mice.Neurochemical research · 2022Article
- Visual Evoked Potentials to Monitor Myelin Cuprizone-Induced Functional Changes.Frontiers in neuroscience · 2022Article
- 2-Methoxyestradiol Alleviates Neuroinflammation and Brain Edema in Early Brain Injury After Subarachnoid Hemorrhage in Rats.Frontiers in cellular neuroscience · 2022Article
- Long Non-coding RNA HOTAIR in Central Nervous System Disorders: New Insights in Pathogenesis, Diagnosis, and Therapeutic Potential.Frontiers in molecular neuroscience · 2022Review
- Effect of β-hydroxybutyrate on behavioral alterations, molecular and morphological changes in CNS of multiple sclerosis mouse model.Frontiers in aging neuroscience · 2022Article
- Cuprizone feed formulation influences the extent of demyelinating disease pathology.Scientific reports · 2021Article
- Oligodendrocyte Lineage Marker Expression in eGFP-GFAP Transgenic Mice.Journal of molecular neuroscience : MN · 2021Article
- Article
- Article
- Microglia and Neuroinflammation: What Place for P2RY12?International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic inflammatory CNS disease, which causes demyelinated lesions and damages white and gray matter regions. Aging is a significant factor in the progression of MS, and microglia, the immune cells of the CNS tissue, play an important role in all disease stages. During aging, microglia are functionally altered. These age-related changes probably already begin early and might influence the progression of CNS pathologies. The aim of the present study was to investigate whether microglia in the middle-aged CNS already react differently to demyelination. For this purpose, several microglia markers (ionized calcium binding adaptor molecule 1 (Iba-1), P2RY12, F4/80, CD68, major histocompatibility complex II (MHCII), macrophage receptor with collagenous structure (Marco), Translocator protein 18 kD (TSPO), CD206, and CD163) were analyzed in the acute cuprizone demyelination model in young (2-month-old) and middle-aged (10-month-old) mice. In addition, microglial proliferation was quantified using double-labeling with proliferating cell nuclear antigen (PCNA) and bromodeoxyuridine (BrdU), which was injected with the onset of remyelination. To compare age-related microglial changes during de- and remyelination in both gray and white matter, the hilus of the dorsal hippocampal dentate gyrus (DG) and the splenium of the corpus callosum (CC) were analyzed in parallel. Age-related changes in microglia of healthy controls were more pronounced in the analyzed gray matter region (higher levels of F4/80 and Marco as well as lower expression of CD68 in middle-aged mice). During de- and remyelination, a stronger increase of the microglial markers Iba-1, CD68 and TSPO was observed in the splenium of the younger groups. There was a significant reduction of P2RY12 during demyelination, however, this was age- and region-dependent. The induction of the anti-inflammatory markers CD206 and CD163 was stronger in the middle-aged group, but also differed between the two analyzed regions. De- and remyelination led to a significant increase in PCNA
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