ArticleMolecular brain2020
Toll-like receptor 4 deficiency ameliorates β2-microglobulin induced age-related cognition decline due to neuroinflammation in mice.
Article in Molecular brain, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
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- Beyond Neuroinflammation: Microglia at the Crossroads of Amyloid, Tau, and Neurodegeneration in Alzheimer's Disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Paracrine Bone-Derived Senescent Secretome Induces Spatially Patterned ECM and Biomechanical Vulnerability in Human Brain Organoids.bioRxiv : the preprint server for biology · 2025Article
- Microglial activation as a hallmark of neuroinflammation in Alzheimer's disease.Metabolic brain disease · 2025Review
- Anti-neuroinflammatory and Neuroprotective Effects of T-006 on Alzheimer's Disease Models by Modulating TLR4-Mediated MyD88/ NF-κB Signaling.CNS & neurological disorders drug targets · 2025Article
- The role of the microbiota-gut-brain axis in schizophrenia: an immunological perspective.Frontiers in immunology · 2025Review
- The relationship between intrinsic capacity and sarcopenia in middle-aged and older Chinese populations: the mediating influence of a novel nutritional index.Frontiers in public health · 2025Article
- Establishment of fracture blister model and analysis of plasma protein markers in rats.Frontiers in immunology · 2025Article
- β2-microglobulin and cognitive decline: unraveling the mediating role of the Dunedin Pace of Aging methylation.Frontiers in aging neuroscience · 2025Article
- Interleukin-6 induces cognitive impairment via toll-like receptor 4 (TLR4)-mediated neuroinflammation and neurodegeneration in mice with chronic kidney disease.Neuroprotection (Chichester, England) · 2024Article
- The Role of Beta2-Microglobulin in Central Nervous System Disease.Cellular and molecular neurobiology · 2024Review
- Correction to: Toll-like receptor 4 deficiency ameliorates β2-microglobulin induced age-related cognition decline due to neuroinflammation in mice.Molecular brain · 2024Article
- Neuroinflammation of Microglial Regulation in Alzheimer's Disease: Therapeutic Approaches.Molecules (Basel, Switzerland) · 2024Review
- J147 ameliorates sepsis-induced depressive-like behaviors in mice by attenuating neuroinflammation through regulating the TLR4/NF-κB signaling pathway.Journal of molecular histology · 2023Article
- Neuronal MHC-I complex is destabilized by amyloid-β and its implications in Alzheimer's disease.Cell & bioscience · 2023Article
- NEK7 inhibition attenuates AβJournal of clinical biochemistry and nutrition · 2023Article
- TRIM62 knockdown by inhibiting the TLR4/NF-κB pathway and NLRP3 inflammasome attenuates cognitive impairment induced by diabetes in mice.Journal of clinical biochemistry and nutrition · 2023Article
- Serum β2-microglobulin is closely associated with 3-month outcome of acute intracerebral hemorrhage: a retrospective cohort study.Irish journal of medical science · 2023Article
- SARS-CoV-2 Spike protein induces TLR4-mediated long-term cognitive dysfunction recapitulating post-COVID-19 syndrome in mice.Cell reports · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 4 (TLR4) is a crucial receptor in neuroinflammation and apoptotic neuronal death, and increasing evidences indicated that β2-microglobulin (B2M) is thought to be a major contributor to age-related cognitive decline. In present study, we designed to investigate the effects of TLR4 on B2M-induced age-related cognitive decline. Wild-type (WT) C57BL/6, TLR4 knockout (TLR4 -KO) mice and hippocampal neurons from the two type mice were respectively divided into two groups: (1) Veh group; (2) B2M-treated group. The behavioral responses of mice were measured using Morris Water Maze. Hippocampal neurogenesis and neuronal damage, inflammatory response, apoptosis, synaptic proteins and neurotrophic factors, and TLR4/MyD88/NF-κB signaling pathway proteins were examined using molecular biological or histopathological methods. The results showed that WT mice received B2M in the DG exhibited age-related cognitive declines, increased TLR4 mRNA expression and high levels of interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α) and apoptotic neuronal death in the hippocampus, which were partially attenuated in TLR4-KO mice. Moreover, in absence of TLR4, B2M treatment improved hippocampus neurogenesis and increased synaptic related proteins. Our cell experiments further demonstrated that deletion of TLR4 could significantly increase synaptic related protein, decrease neuroinflammatory fators, inhibited apoptotic neuronal death, and regulated MyD88/NF-κB signal pathway after B2M treatment. In summary, our results support the TLR4 contributes to B2M-induced age-related cognitive decline due to neuroinflammation and apoptosis through TLR4/MyD88/NF-κB signaling pathway via a modulation of hippocampal neurogenesis and synaptic function. This may provide an important neuroprotective mechanism for improving age-related cognitive decline.
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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.