ArticleExperimental neurology2011
High-mobility group box-1 impairs memory in mice through both toll-like receptor 4 and Receptor for Advanced Glycation End Products.
Article in Experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07469748 (Development, Validity and Reliability Study of the Health Belief Model Scale Regarding Disability and Abilities in Vestibular Migraine Patients), which is not on this map. Cited by 84 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Development, Validity and Reliability Study of the Health Belief Model Scale Regarding Disability and Abilities in Vestibular Migraine Patients
Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 181 citations in OpenAlex.
- The Role of High Mobility Group Box 1 (HMGB1) in Neurodegeneration: A Systematic Review.Current neuropharmacology · 2022Pooled it
- Epilepsy as a Disorder of Neuroimmune Metabolism: The Kynurenine Pathway as a Link Between Cognitive and Psychiatric Dysfunction.Biomolecules · 2026Review
- Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026Review
- Clinical and biochemical assessments of circulating High Mobility Group Box Protein1 in children with epilepsy: relation to cognitive function and drug responsiveness.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Roles of the Receptor for Advanced Glycation End Products and Its Ligands in the Pathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2025Review
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Lupus autoantibodies initiate neuroinflammation sustained by continuous HMGB1:RAGE signaling and reversed by increased LAIR-1 expression.Nature immunology · 2024Article
- The HMGB1-RAGE axis in nucleus accumbens facilitates cocaine-induced conditioned place preference via modulating microglial activation.Brain and behavior · 2024Article
- Article
- Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.PeerJ · 2024Article
- Genetic variants in the TAC1 transcriptional regulatory region affect on trainability and excitability levels in Belgian Malinois dogs.Veterinary medicine and science · 2024Article
- Intracellular DAMPs in Neurodegeneration and Their Role in Clinical Therapeutics.Molecular neurobiology · 2023Review
- Effects of Diabetes Mellitus-Related Dysglycemia on the Functions of Blood-Brain Barrier and the Risk of Dementia.International journal of molecular sciences · 2023Review
- Receptors for Advanced Glycation End Products (RAGE): Promising Targets Aiming at the Treatment of Neurodegenerative Conditions.Current neuropharmacology · 2023Review
- Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease.Journal of neuroinflammation · 2022Review
- Cattle BileFrontiers in pharmacology · 2022Article
- Ethyl Pyruvate Alleviating Inflammatory Response after Diabetic Cerebral Hemorrhage.Current neurovascular research · 2022Article
- Toll-Like Receptor 4: A Promising Therapeutic Target for Alzheimer's Disease.Mediators of inflammation · 2022Review
- Chronic Intestinal Inflammation Suppresses Brain Activity by Inducing Neuroinflammation in Mice.The American journal of pathology · 2022Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
High-mobility group box-1 (HMGB1) is a nuclear protein with cytokine-type functions upon its extracellular release. HMGB1 activates inflammatory pathways by stimulating multiple receptors, chiefly toll-like receptor 4 (TLR4) and Receptor for Advanced Glycation End Products (RAGE). TLR4 and RAGE activation has been implicated in memory impairments, although the endogenous ligand subserving these effects is unknown. We examined whether HMGB1 induced memory deficits using novel object recognition test, and which of the two receptor pathways was involved in these effects. Non-spatial long-term memory was examined in wild type, TLR4 knockout, and RAGE knockout mice. Recombinant HMGB1 (10μg, intracerebroventricularly, i.c.v.) disrupted memory encoding equipotently in wild type, TLR4 knockout and RAGE knockout animals, but affected neither memory consolidation, nor retrieval. Neither TLR4 knockout nor RAGE knockout mice per se, exhibited memory deficits. Blockade of TLR4 in RAGE knockout mice using Rhodobacter sphaeroides lipopolysaccharide (LPS-Rs; 20 μg, i.c.v.) prevented the detrimental effect of HMGB1 on memory. These data show that elevated brain levels of HMGB1 induce memory abnormalities which may be mediated by either TLR4, or RAGE. This mechanism may contribute to memory deficits under various neurological and psychiatric conditions associated with the increased HMGB1 levels, such as epilepsy, Alzheimer's disease and stroke.
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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.