ArticleBrain, behavior, and immunity2013
Loss of astrocytic leptin signaling worsens experimental autoimmune encephalomyelitis.
Article in Brain, behavior, and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Leptin as a Potential Modifier of Neuroinflammation: Contrasting Roles in Alzheimer's Disease and Multiple Sclerosis.International journal of molecular sciences · 2025Review
- The Role of Adipokines in the Pathologies of the Central Nervous System.International journal of molecular sciences · 2023Review
- Adipokines as Immune Cell Modulators in Multiple Sclerosis.International journal of molecular sciences · 2021Review
- Tissue plasminogen activator worsens experimental autoimmune encephalomyelitis by complementary actions on lymphoid and myeloid cell responses.Journal of neuroinflammation · 2021Article
- Hormones in experimental autoimmune encephalomyelitis (EAE) animal models.Translational neuroscience · 2021Review
- Impact of Metabolic Syndrome on Neuroinflammation and the Blood-Brain Barrier.Frontiers in neuroscience · 2018Review
- From blood-brain barrier to blood-brain interface: new opportunities for CNS drug delivery.Nature reviews. Drug discovery · 2016Review
- Peptides and the blood-brain barrier.Peptides · 2015Review
- Astrocyte response to IFN-γ limits IL-6-mediated microglia activation and progressive autoimmune encephalomyelitis.Journal of neuroinflammation · 2015Article
- Leukocyte infiltration into spinal cord of EAE mice is attenuated by removal of endothelial leptin signaling.Brain, behavior, and immunity · 2014Article
- Leukocyte infiltration across the blood-spinal cord barrier is modulated by sleep fragmentation in mice with experimental autoimmune encephalomyelitis.Fluids and barriers of the CNS · 2014Article
- The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis.Multiple sclerosis international · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Leptin is commonly thought to play a detrimental role in exacerbating experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis. Paradoxically, we show here that astrocytic leptin signaling has beneficial effects in reducing disease severity. In the astrocyte specific leptin receptor knockout (ALKO) mouse in which leptin signaling is absent in astrocytes, there were higher EAE scores (more locomotor deficits) than in the wildtype counterparts. The difference mainly occurred at a late stage of EAE when wildtype mice showed signs of recovery whereas ALKO mice continued to deteriorate. The more severe symptoms in ALKO mice coincided with more infiltrating cells in the spinal cord and perivascular brain parenchyma, more demyelination, more infiltrating CD4 cells, and a lower percent of neutrophils in the spinal cord 28 days after EAE induction. Cultured astrocytes from wildtype mice showed increased adenosine release in response to interleukin-6 and the hippocampus of wildtype mice had increased adenosine production 28 days after EAE induction, but the ALKO mutation abolished the increase in both conditions. This indicates a role of astrocytic leptin in normal gliotransmitter release and astrocyte functions. The worsening of EAE in the ALKO mice in the late stage suggests that astrocytic leptin signaling helps to clear infiltrating leukocytes and reduce autoimmune destruction of the CNS.
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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.