ReviewBrain sciences2021
TLR-Mediated Signal Transduction and Neurodegenerative Disorders.
Review in Brain sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Molecular Mechanisms Between Canine Parvovirus 2 and Host Interactions: From Viruses to Innate Immune Signaling Pathways.Viruses · 2026Review
- Let-7a-5p/SHIP-1 Axis Drives SARS-CoV-2 Spike-1-Induced Microglial Pyroptosis.International journal of molecular sciences · 2026Article
- Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- Central Role of Toll-like Receptor-9 Gene Function in Inflammation-Mediated Neuronal Plasticity: Implications for Long-Term Memory Development.Molecular neurobiology · 2025Review
- Machine Learning Integration of Bulk and Single-Cell RNA-Seq Data Reveals Cathepsin B as a Central PANoptosis Regulator in Influenza.International journal of molecular sciences · 2025Article
- Parkinson's disease: exploring the systemic immune mechanisms through molecular investigations.Inflammopharmacology · 2025Review
- Let-7 Family as a Mediator of Exercise on Alzheimer's Disease.Cellular and molecular neurobiology · 2025Review
- Korean black ginseng extract alleviates Alzheimer's disease-related cognitive impairment by activating the Nrf2/HO-1 pathway and suppressing the p38 MAPK/NF-κB/STAT3 pathways and NLRP3 inflammasome via TLR2 and TLR4 modulation.Journal of ginseng research · 2025Article
- Viruses and neurodegeneration: a growing concern.Journal of translational medicine · 2025Review
- Intestinal-pulmonary axis: a 'Force For Good' against respiratory viral infections.Frontiers in immunology · 2025Review
- Article
- Distinct neuroprotective and anti-inflammatory effects of Kampo formulas ninjinyoeito and juzentaihoto in depression-like SAMP8 mice.Frontiers in pharmacology · 2025Article
- A neurotrophin functioning with a Toll regulates structural plasticity in a dopaminergic circuit.eLife · 2024Article
- Kinin BInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Neuroinflammaging: A Tight Line Between Normal Aging and Age-Related Neurodegenerative Disorders.Aging and disease · 2024Review
- Aloesin ameliorates hypoxic-ischemic brain damage in neonatal mice by suppressing TLR4-mediated neuroinflammation.Immunity, inflammation and disease · 2024Article
- Mitigating neurodegenerative diseases: the protective influence of baicalin and baicalein through neuroinflammation regulation.Frontiers in pharmacology · 2024Review
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Mitochondrial DNA and Inflammation in Alzheimer's Disease.Current issues in molecular biology · 2023Review
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A special class of proteins called Toll-like receptors (TLRs) are an essential part of the innate immune system, connecting it to the adaptive immune system. There are 10 different Toll-Like Receptors that have been identified in human beings. TLRs are part of the central nervous system (CNS), showing that the CNS is capable of the immune response, breaking the long-held belief of the brain's "immune privilege" owing to the blood-brain barrier (BBB). These Toll-Like Receptors are present not just on the resident macrophages of the central nervous system but are also expressed by the neurons to allow them for the production of proinflammatory agents such as interferons, cytokines, and chemokines; the activation and recruitment of glial cells; and their participation in neuronal cell death by apoptosis. This study is focused on the potential roles of various TLRs in various neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD), namely TLR2, TLR3, TLR4, TLR7, and TLR9 in AD and PD in human beings and a mouse model.
Indexed as
Identifiers
What Socratic 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 Socratic graph.