ArticleMetabolic brain disease2017
DRα1-MOG-35-55 treatment reduces lesion volumes and improves neurological deficits after traumatic brain injury.
Article in Metabolic brain disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Neuronal and glial networks interact with traumatic brain injury to modulate cognition in ABCD study.NPJ systems biology and applications · 2026Article
- Decoding hippocampal subfield and glial responses in ischemia using single-cell transcriptomics.Journal of translational medicine · 2025Article
- Novel therapeutic for multiple sclerosis protects white matter function in EAE mouse model.Frontiers in molecular medicine · 2023Article
- A Novel Partial MHC Class II Construct, DRmQ, Inhibits Central and Peripheral Inflammatory Responses to Promote Neuroprotection in Experimental Stroke.Translational stroke research · 2020Article
- Spleen participation in partial MHC class II construct neuroprotection in stroke.CNS neuroscience & therapeutics · 2020Review
- VX765 Attenuates Pyroptosis and HMGB1/TLR4/NF-Oxidative medicine and cellular longevity · 2020Article
- Edaravone attenuates traumatic brain injury through anti-inflammatory and anti-oxidative modulation.Experimental and therapeutic medicine · 2019Article
- A novel neurotherapeutic for multiple sclerosis, ischemic injury, methamphetamine addiction, and traumatic brain injury.Journal of neuroinflammation · 2019Review
- Potential immunotherapies for traumatic brain and spinal cord injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018Review
- Huperzine A alleviates neuroinflammation, oxidative stress and improves cognitive function after repetitive traumatic brain injury.Metabolic brain disease · 2017Article
- Major histocompatibility complex Class II-based therapy for stroke.Brain circulationReview
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury (TBI) results in severe neurological impairments without effective treatments. Inflammation appears to be an important contributor to key pathogenic events such as secondary brain injury following TBI and therefore serves as a promising target for novel therapies. We have recently demonstrated the ability of a molecular construct comprised of the human leukocyte antigen (HLA)-DRα1 domain linked covalently to mouse (m)MOG-35-55 peptide (DRα1-MOG-35-55 construct) to reduce CNS inflammation and tissue injury in animal models of multiple sclerosis and ischemic stroke. The aim of the current study was to determine if DRα1-MOG-35-55 treatment of a fluid percussion injury (FPI) mouse model of TBI could reduce the lesion size and improve disease outcome measures. Neurodeficits, lesion size, and immune responses were determined to evaluate the therapeutic potential and mechanisms of neuroprotection induced by DRα1-MOG-35-55 treatment. The results demonstrated that daily injections of DRα1-MOG-35-55 given after FPI significantly reduced numbers of infiltrating CD74
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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.