ArticleGlia2016
Juvenile striatal white matter is resistant to ischemia-induced damage.
Article in Glia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- NG2-Glia in Central Nervous System Following Injury: From Pathological Involvement to Repair Potential.CNS neuroscience & therapeutics · 2026Review
- TNF-α/PAD4 axis drives hyperhomocysteine-induced white matter injury after acute ischemic stroke.Acta pharmacologica Sinica · 2026Article
- Reactive OPCs in CNS Injury: From Functional Diversity to Therapeutic Translation.Neuroscience bulletin · 2026Review
- Mechanism-Oriented Treatment of Early Neurologic Deterioration in Acute Ischemic Stroke.Journal of stroke · 2026Review
- Changing genes, cells and networks to reprogram the brain after stroke.Nature neuroscience · 2025Review
- Single-Cell Analysis in Cerebrovascular Research: Primed for Breakthroughs and Clinical Impact.Stroke · 2025Review
- Brain Maturation as a Fundamental Factor in Immune-Neurovascular Interactions in Stroke.Translational stroke research · 2024Review
- Perspective from single-cell sequencing: Is inflammation in acute ischemic stroke beneficial or detrimental?CNS neuroscience & therapeutics · 2024Review
- Neuroimmune Support of Neuronal Regeneration and Neuroplasticity following Cerebral Ischemia in Juvenile Mice.Brain sciences · 2023Article
- A Novel Ex Vivo Model to Study Therapeutic Treatments for Myelin Repair following Ischemic Damage.International journal of molecular sciences · 2023Article
- The Role of Infection and Inflammation in the Pathogenesis of Pediatric Arterial Ischemic Stroke.Seminars in pediatric neurology · 2022Review
- Cerebral ischemia in the developing brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- The Notch Signaling Pathway Regulates Differentiation of NG2 Cells into Oligodendrocytes in Demyelinating Diseases.Cellular and molecular neurobiology · 2022Review
- Role of Glial Cell-Derived Oxidative Stress in Blood-Brain Barrier Damage after Acute Ischemic Stroke.Oxidative medicine and cellular longevity · 2022Review
- Oligodendrocyte Lineage Marker Expression in eGFP-GFAP Transgenic Mice.Journal of molecular neuroscience : MN · 2021Article
- Microglia-leucocyte axis in cerebral ischaemia and inflammation in the developing brain.Acta physiologica (Oxford, England) · 2021Review
- Review
- The roles of neuron-NG2 glia synapses in promoting oligodendrocyte development and remyelination.Cell and tissue research · 2020Review
- Experimental pediatric stroke shows age-specific recovery of cognition and role of hippocampal Nogo-A receptor signaling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
White matter injury following ischemic stroke is a major cause of functional disability. Injury to both myelinated axons and oligodendrocytes, the myelin producing cells in the central nervous system, occurs in experimental models of ischemic stroke. Age-related changes in white matter vulnerability to ischemia have been extensively studied and suggest that both the perinatal and the aged periods are times of increased white matter vulnerability. However, sensitivity of white matter following stroke in the juvenile brain has not been evaluated. Interestingly, the late pediatric period is an important developmental stage, as it is the time of maximal myelination. The current study demonstrates that neurons in late pediatric/juvenile striatum are vulnerable to ischemic damage, with neuronal injury being comparable in juvenile and adult mice following ischemia. By contrast, actively myelinating striatal oligodendrocytes in the juvenile brain are resistant to ischemia, whereas adult oligodendrocytes are quite sensitive. As a result, myelin sheaths are remarkably intact and axons survive well in the injured striatum of juvenile mice. In addition to relative resistance of juvenile white matter, other glial responses were very different in juvenile and adult mice following cerebral ischemia, including differences in astrogliosis, fibrosis, NG2-cell reactivity, and vascular integrity. Together, these responses lead to long-term preservation of brain parenchyma in juvenile mice, compared to severe tissue loss and scarring in adult mice. Overall, the current study suggests that equivalent ischemic insults may result in less functional deficit in children compared to adults and an environment more conducive to long-term recovery. GLIA 2016;64:1972-1986.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.