ArticleAging2019
Genomic deletion of TLR2 induces aggravated white matter damage and deteriorated neurobehavioral functions in mouse models of Alzheimer's disease.
Article in Aging, 2019. 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, 56 citations in OpenAlex.
- Diffusion MRI reveals amyloid plaque-associated cellular signatures through spatial transcriptomic integration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026Review
- Late-Stage Activation of Toll-like receptor 3 Alleviates Cognitive Impairment and Neuropathology in an Alzheimer's Disease Mouse Model.Molecular neurobiology · 2025Article
- The Interplay of Inflammation and Gut-Microbiota Dysbiosis in Alzheimer's Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Investigation of Novel Aronia Bioactive Fraction-Alginic Acid Nanocomplex on the Enhanced Modulation of Neuroinflammation and Inhibition of Aβ Aggregation.Pharmaceutics · 2024Article
- Loss of microRNA-15a/16-1 function promotes neuropathological and functional recovery in experimental traumatic brain injury.JCI insight · 2024Article
- From Immunity to Neurogenesis: Toll-like Receptors as Versatile Regulators in the Nervous System.International journal of molecular sciences · 2024Review
- Repurposing non-pharmacological interventions for Alzheimer's disease through link prediction on biomedical literature.Scientific reports · 2024Article
- Review
- Immune receptors and aging brain.Bioscience reports · 2024Review
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
- Gain-of-function of progesterone receptor membrane component 2 ameliorates ischemic brain injury.CNS neuroscience & therapeutics · 2023Article
- Early activation of Toll-like receptor-3 reduces the pathological progression of Alzheimer's disease in APP/PS1 mouse.Alzheimer's research & therapy · 2023Article
- The effects of microglia-associated neuroinflammation on Alzheimer's disease.Frontiers in immunology · 2023Review
- Genetic deletion of Krüppel-like factor 11 aggravates traumatic brain injury.Journal of neuroinflammation · 2022Article
- Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Identification of Biomarkers Related to M2 Macrophage Infiltration in Alzheimer's Disease.Cells · 2022Article
- Genetic Deficiency of MicroRNA-15a/16-1 Confers Resistance to Neuropathological Damage and Cognitive Dysfunction in Experimental Vascular Cognitive Impairment and Dementia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Protective Effects of Polysaccharides in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- Bacterial Amyloid Curli Associated Gut Epithelial Neuroendocrine Activation Predominantly Observed in Alzheimer's Disease Mice with Central Amyloid-β Pathology.Journal of Alzheimer's disease : JAD · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor-2 (TLR2), a member of the TLR family, plays an important role in the initiation and regulation of immune/inflammation response, which is a critical mechanism underlying Alzheimer's disease (AD). To clarify the role of TLR2 in the pathological process of AD, in the present study, TLR2 knockout plus APPswe/PSEN1dE9 transgenic mice (AD-TLR2KO) were generated. Neurobehavioral tests and brain MRI scan were conducted on mice at the age of 12 months. Additionally, neuron loss was evaluated using NeuN staining. Amyloid β protein (Aβ), glial fibrillary acidic protein (GFAP), endogenous ligands for TLR2, and the activation of downstream signaling of TLR2 in mouse brains were detected by immunohistochemistry and Western blots. The results demonstrated that TLR2 deficit induced learning disabilities, decreased spontaneous activity, increased anxiety and depression, and led to white matter damage (WMD), brain atrophy, loss of neurons, and glial activation. Moreover, TLR2 deficit aggravated impaired neurobehavioral functions and WMD in AD mice, but did not affect the Aβ deposition in mouse brains. Our data indicate that the genomic deletion of TLR2 impairs neurobehavioral functions, induces WMD and brain atrophy, and increases the activation of astrocytes, which in turn aggravate the symptoms of AD through a non-Aβ mechanism.
Indexed as
Identifiers
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.