ReviewInternational immunopharmacology2011
Toll-like receptors are key players in neurodegeneration.
Review in International immunopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 114 citations in OpenAlex.
- Myd88 Deficiency Accelerates Retinal Degeneration and Alters Microglial Dynamics in a Mouse Model of Retinitis Pigmentosa.Investigative ophthalmology & visual science · 2026Article
- PROTAC-mediated multi-target protein degradation in Alzheimer's disease: mechanistic insights, therapeutic applications, and translational challenges.RSC medicinal chemistry · 2026Review
- Chemical Exchange Saturation Transfer Imaging in Neuroinflammation: Methods, Challenges, and Recommendations.International journal of molecular sciences · 2025Review
- Repurposing Sigma-1 Receptor-Targeting Drugs for Therapeutic Advances in Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Drugless peptide-based nanohybrids alleviate diabetic retinopathy by suppressing microglial activation and endothelial inflammation.Theranostics · 2025Article
- Mechanistic insights on TLR-4 mediated inflammatory pathway in neurodegenerative diseases.Pharmacological reports : PR · 2024Review
- Therapeutic Correlation of TLR-4 Mediated NF-κB Inflammatory Pathways in Ischemic Injuries.Current drug targets · 2024Review
- Article
- Oxidative Stress as a Potential Mechanism Underlying Membrane Hyperexcitability in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Biological Potential, Gastrointestinal Digestion, Absorption, and Bioavailability of Algae-Derived Compounds with Neuroprotective Activity: A Comprehensive Review.Marine drugs · 2022Review
- P2Y6 receptor-mediated signaling amplifies TLR-induced pro-inflammatory responses in microglia.Frontiers in immunology · 2022Article
- Microglia and Neuroinflammation: Crucial Pathological Mechanisms in Traumatic Brain Injury-Induced Neurodegeneration.Frontiers in aging neuroscience · 2022Review
- The anti-inflammatory effects of cinnamyl alcohol on sepsis-induced mice via the NLRP3 inflammasome pathway.Annals of translational medicine · 2022Article
- NEU1-A Unique Therapeutic Target for Alzheimer's Disease.Frontiers in pharmacology · 2022Review
- The Innate and Adaptive Immune Cells in Alzheimer's and Parkinson's Diseases.Oxidative medicine and cellular longevity · 2022Review
- Toll-Like Receptor Signaling Pathways: Novel Therapeutic Targets for Cerebrovascular Disorders.International journal of molecular sciences · 2021Review
- Differential expression of genes involved in the acute innate immune response to intracortical microelectrodes.Acta biomaterialia · 2020Article
- Lack of TLR4 modifies the miRNAs profile and attenuates inflammatory signaling pathways.PloS one · 2020Article
- Dysregulation of TLR5 and TAM Ligands in the Alzheimer's Brain as Contributors to Disease Progression.Molecular neurobiology · 2019Article
- Imbalance of Microglial TLR4/TREM2 in LPS-Treated APP/PS1 Transgenic Mice: A Potential Link Between Alzheimer's Disease and Systemic Inflammation.Neurochemical research · 2019Article
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 1 country.
Funding
Abstract
The activation of innate immune response is initiated by engagement of pattern-recognition receptors (PPRs), such as Toll-like receptors (TLRs). These receptors are expressed in peripheral leukocytes and in many cell types in the central nervous system (CNS). The expression of TLRs in CNS was mainly studied in astrocytes and microglial cells. However, new evidence indicates that these receptors may play an important role in neuronal homeostasis. The expression of TLRs in the CNS is variable and can be modulated by multiple factors, including pro-inflammatory molecules, which are elevated in neurodegenerative diseases and can increase the expression of TLRs in CNS cells. Moreover, activation of TLRs induces the release of pro-inflammatory cytokines. Therefore, TLRs have been shown to play a role in several aspects of neurodegenerative diseases. Here we will discuss results reported in the recent literature concerning the participation of TLRs in neurodegenerative diseases.
Indexed as
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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.