ArticleHeliyon2018
Deficiency of Toll-like receptors 2, 3 or 4 extends life expectancy in Huntington's disease mice.
Article in Heliyon, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Exploration of the genetic neuroinflammatory environment in the human midcingulate cortex in Huntington's disease.Communications medicine · 2026Article
- Pathophysiological role of high mobility group box-1 signaling in neurodegenerative diseases.Inflammopharmacology · 2025Review
- Innate Immune Mechanisms in the Central Nervous System.Advances in experimental medicine and biology · 2025Review
- Tremendous Fidelity of Vitamin D3 in Age-related Neurological Disorders.Molecular neurobiology · 2024Review
- Mechanistic insights on TLR-4 mediated inflammatory pathway in neurodegenerative diseases.Pharmacological reports : PR · 2024Review
- The role of neuroinflammation in neurodegenerative diseases: current understanding and future therapeutic targets.Frontiers in aging neuroscience · 2024Review
- Naïve Huntington's disease microglia mount a normal response to inflammatory stimuli but display a partially impaired development of innate immune tolerance that can be counteracted by ganglioside GM1.Journal of neuroinflammation · 2023Article
- Toll-Like Receptor 4 Plays a Significant Role in the Biochemical and Neurological Alterations Observed in Two Distinct Mice Models of Huntington's Disease.Molecular neurobiology · 2023Article
- Toll-like receptors in pathogenesis of neurodegenerative diseases and their therapeutic potential.Immunity, inflammation and disease · 2023Review
- Biological Potential, Gastrointestinal Digestion, Absorption, and Bioavailability of Algae-Derived Compounds with Neuroprotective Activity: A Comprehensive Review.Marine drugs · 2022Review
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- Inhibitory Effect of Trihydroxy Isoflavone on Neuronal Apoptosis in Natural Aging Rats.Disease markers · 2022Article
- Proteopathic tau primes and activates interleukin-1β via myeloid-cell-specific MyD88- and NLRP3-ASC-inflammasome pathway.Cell reports · 2021Article
- Toll-Like Receptor Signaling Pathways: Novel Therapeutic Targets for Cerebrovascular Disorders.International journal of molecular sciences · 2021Review
- Phosphoinositides: Roles in the Development of Microglial-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- How Do Post-Translational Modifications Influence the Pathomechanistic Landscape of Huntington's Disease? A Comprehensive Review.International journal of molecular sciences · 2020Review
- Association Between Toll-Like Receptor 4 (TLR4) and Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) Genetic Variants and Clinical Progression of Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2020Article
- Exploring the role of high-mobility group box 1 (HMGB1) protein in the pathogenesis of Huntington's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Neurodegenerative diseases have genetic hallmarks of autoinflammatory disease.Human molecular genetics · 2018Review
- Role of Microglia TLRs in Neurodegeneration.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
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD), an autosomal dominant neurodegenerative disorder characterized by progressive striatal and cortical atrophy, has been strongly linked with neuroinflammation. Toll-like receptors, a family of innate immune receptors, are a major pathway for neuroinflammation with pleiotropic effects on neuronal plasticity and neurodevelopment. We assessed whether deficiency for TLRs 2, 3 or 4 affects life expectancy in the N171-82Q mouse model of HD. Our data indicate that homozygous TLRs 2 and 3 as well as heterozygous TLR4 deficiency significantly extends the life expectancy of HD mice. Our data suggest that multiple TLR pathways may be involved in the neuroinflammatory and degenerative processes during HD.
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What OpenQuestion holds
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.