ArticleNeuromolecular medicine2014
Interleukin-1β promotes long-term potentiation in patients with multiple sclerosis.
Article in Neuromolecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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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.
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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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Early diagnosis of secondary progressive multiple sclerosis: focus on fluid and neurophysiological biomarkers.Journal of neurology · 2021Pooled it
- Interleukin-1β Alters Hebbian Synaptic Plasticity in Multiple Sclerosis.International journal of molecular sciences · 2020Trial
- Glia Connect Inflammation and Neurodegeneration in Multiple Sclerosis.Neuroscience bulletin · 2023Review
- Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023Review
- The Inflammatory Signals Associated with Psychosis: Impact of Comorbid Drug Abuse.Biomedicines · 2023Review
- Tumor-related molecular determinants of neurocognitive deficits in patients with diffuse glioma.Neuro-oncology · 2022Article
- Article
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- The role of gut-immune-brain signaling in substance use disorders.International review of neurobiology · 2021Article
- Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis.Frontiers in cellular neuroscience · 2020Review
- Modeling Resilience to Damage in Multiple Sclerosis: Plasticity Meets Connectivity.International journal of molecular sciences · 2019Review
- Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTPβ/ζ Axis: Relevance in Therapeutic Development.Frontiers in pharmacology · 2019Review
- Mechanisms of neurobehavioral abnormalities in multiple sclerosis: Contributions from neural and immune components.Clinical neurophysiology practice · 2019Review
- Principles of inflammasome priming and inhibition: Implications for psychiatric disorders.Brain, behavior, and immunity · 2018Review
- Depression following a traumatic brain injury: uncovering cytokine dysregulation as a pathogenic mechanism.Neural regeneration research · 2018Review
- Platelet-derived growth factor predicts prolonged relapse-free period in multiple sclerosis.Journal of neuroinflammation · 2018Article
- Tumor Necrosis Factor and Interleukin-1Neural plasticity · 2018Review
- Interplay Between Age and Neuroinflammation in Multiple Sclerosis: Effects on Motor and Cognitive Functions.Frontiers in aging neuroscience · 2018Review
- Neuroimmune Activation Drives Multiple Brain States.Frontiers in systems neuroscience · 2018Review
- TRPV4 Inhibition Improved Myelination and Reduced Glia Reactivity and Inflammation in a Cuprizone-Induced Mouse Model of Demyelination.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune system shapes synaptic transmission and plasticity in experimental autoimmune encephalomyelitis (EAE), the mouse model of multiple sclerosis (MS). These synaptic adaptations are believed to drive recovery of function after brain lesions, and also learning and memory deficits and excitotoxic neurodegeneration; whether inflammation influences synaptic plasticity in MS patients is less clear. In a cohort of 59 patients with MS, we found that continuous theta-burst transcranial magnetic stimulation did not induce the expected long-term depression (LTD)-like synaptic phenomenon, but caused persisting enhancement of brain cortical excitability. The amplitude of this long-term potentiation (LTP)-like synaptic phenomenon correlated with the concentration of the pro-inflammatory cytokine interleukin-1β (IL-1β) in the cerebrospinal fluid. In MS and EAE, the brain and spinal cord are typically enriched of CD3(+) T lymphocyte infiltrates, which are, along with activated microglia and astroglia, a major cause of inflammation. Here, we found a correlation between the presence of infiltrating T lymphocytes in the hippocampus of EAE mice and synaptic plasticity alterations. We observed that T lymphocytes from EAE, but not from control mice, release IL-1β and promote LTP appearance over LTD, thereby mimicking the facilitated LTP induction observed in the cortex of MS patients. EAE-specific T lymphocytes were able to suppress GABAergic transmission in an IL-1β-dependent manner, providing a possible synaptic mechanism able to lower the threshold of LTP induction in MS brains. Moreover, in vivo blockade of IL-1β signaling resulted in inflammation and synaptopathy recovery in EAE hippocampus. These data provide novel insights into the pathophysiology of MS.
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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.