ArticleActa neuropathologica communications2014
Amyloid β and Tau Alzheimer's disease related pathology is reduced by Toll-like receptor 9 stimulation.
Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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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.
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Who cites it
58 citing papers in PubMed, 77 citations in OpenAlex.
- DNA Sensing Pathways in Innate Immunity: Implications for Alzheimer's Disease Progression and Therapy.Molecular neurobiology · 2026Review
- Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026Review
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Immune modulation to treat Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease.Cells · 2025Review
- Microglial modulation as a therapeutic strategy in Alzheimer's disease: Focus on microglial preconditioning approaches.Journal of cellular and molecular medicine · 2024Review
- Immune receptors and aging brain.Bioscience reports · 2024Review
- TLR4-mediated chronic neuroinflammation has no effect on tangle pathology in a tauopathy mouse model.Frontiers in aging neuroscience · 2024Article
- Mutated Toll-like receptor 9 increases Alzheimer's disease risk by compromising innate immunity protection.Molecular psychiatry · 2023Article
- Mitochondrial DNA and Inflammation in Alzheimer's Disease.Current issues in molecular biology · 2023Review
- Article
- The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer's Disease: New Potential Treatment Target.International journal of molecular sciences · 2023Review
- Host immune responses in the central nervous system during fungal infections.Immunological reviews · 2022Review
- TRIOBP-1 Protein Aggregation Exists in Both Major Depressive Disorder and Schizophrenia, and Can Occur through Two Distinct Regions of the Protein.International journal of molecular sciences · 2022Article
- Toll-like receptor-mediated neuroinflammation: relevance for cognitive dysfunctions.Trends in pharmacological sciences · 2022Review
- Improved Spatial Memory And Neuroinflammatory Profile Changes in Aged Rats Submitted to Photobiomodulation Therapy.Cellular and molecular neurobiology · 2022Article
- p38α-MAPK-deficient myeloid cells ameliorate symptoms and pathology of APP-transgenic Alzheimer's disease mice.Aging cell · 2022Article
- Proteostasis Perturbations and Their Roles in Causing Sterile Inflammation and Autoinflammatory Diseases.Cells · 2022Review
- Targeting whole body metabolism and mitochondrial bioenergetics in the drug development for Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- The Lymphatic System in Neurological Disease and Alzheimer's Disease. A Brief Editorial.Current Alzheimer research · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common cause of dementia, and currently, there is no effective treatment. The major neuropathological lesions in AD are accumulation of amyloid β (Aβ) as amyloid plaques and congophilic amyloid angiopathy, as well as aggregated tau in the form of neurofibrillary tangles (NFTs). In addition, inflammation and microglia/macrophage function play an important role in AD pathogenesis. We have hypothesized that stimulation of the innate immune system via Toll-like receptor 9 (TLR9) agonists, such as type B CpG oligodeoxynucleotides (ODNs), might be an effective way to ameliorate AD related pathology. We have previously shown in the Tg2576 AD model that CpG ODN can reduce amyloid deposition and prevent cognitive deficits. In the present study, we used the 3xTg-AD mice with both Aβ and tau related pathology. The mice were divided into 2 groups treated from 7 to 20 months of age, prior to onset of pathology and from 11 to 18 months of age, when pathology is already present. We demonstrated that immunomodulatory treatment with CpG ODN reduces both Aβ and tau pathologies, as well as levels of toxic oligomers, in the absence of any apparent inflammatory toxicity, in both animal groups. This pathology reduction is associated with a cognitive rescue in the 3xTg-AD mice. Our data indicate that modulation of microglial function via TLR9 stimulation is effective at ameliorating all the cardinal AD related pathologies in an AD mouse model suggesting such an approach would have a greater chance of achieving clinical efficacy.
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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.