ArticlePloS one2012
Toxoplasma gondii infection in the brain inhibits neuronal degeneration and learning and memory impairments in a murine model of Alzheimer's disease.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Association between microbiological risk factors and neurodegenerative disorders: An umbrella review of systematic reviews and meta-analyses.Frontiers in psychiatry · 2022Pooled it
- Attenuation of Tau Hyperphosphorylation by Chronic Toxoplasma gondii Infection in a Mouse Model of Alzheimer's Disease.Parasite immunology · 2026Article
- Association between Toxoplasma gondii seropositivity and Alzheimer's disease: a case-control study.Parasitology research · 2026Article
- Toxoplasma gondii drives myeloid immune cell recruitment to amyloid plaques in Alzheimer's model mice.Journal of neuroinflammation · 2026Article
- Article
- Beyond Latency: ChronicBiomedicines · 2025Review
- The Role of Genetic, Environmental, and Dietary Factors in Alzheimer's Disease: A Narrative Review.International journal of molecular sciences · 2025Review
- Toxoplasma gondii Infection of Alzheimer's Disease Mice Reduces Brain Amyloid Density Globally and Regionally.The Journal of infectious diseases · 2024Article
- Contribution of CNS and extra-CNS infections to neurodegeneration: a narrative review.Journal of neuroinflammation · 2024Review
- Inhibition of Foxp3 expression in the placenta of mice infected intraperitoneally by toxoplasma gondii tachyzoites: insights into the PPARγ/miR-7b-5p/Sp1 signaling pathway.Parasites & vectors · 2024Article
- mFrontiers in cell and developmental biology · 2024Review
- Alzheimer's disease and infectious agents: a comprehensive review of pathogenic mechanisms and microRNA roles.Frontiers in neuroscience · 2024Review
- A parasite odyssey: An RNA virus concealed inVirus evolution · 2024Article
- Infectious origin of Alzheimer's disease: Amyloid beta as a component of brain antimicrobial immunity.PLoS pathogens · 2022Review
- Glimepiride mitigates tauopathy and neuroinflammation in P301S transgenic mice: role of AKT/GSK3β signaling.Inflammopharmacology · 2022Article
- Comprehensive Overview ofPathogens (Basel, Switzerland) · 2021Review
- Toxoplasma gondii infection and its implications within the central nervous system.Nature reviews. Microbiology · 2021Review
- Review
- Reduction of Amyloid Burden by Proliferated Homeostatic Microglia inInternational journal of molecular sciences · 2021Article
- Neurological and Neurobehavioral Disorders Associated withJournal of parasitology research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunosuppression is a characteristic feature of Toxoplasma gondii-infected murine hosts. The present study aimed to determine the effect of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of Alzheimer's disease (AD) in Tg2576 AD mice. Mice were infected with a cyst-forming strain (ME49) of T. gondii, and levels of inflammatory mediators (IFN-γ and nitric oxide), anti-inflammatory cytokines (IL-10 and TGF-β), neuronal damage, and β-amyloid plaque deposition were examined in brain tissues and/or in BV-2 microglial cells. In addition, behavioral tests, including the water maze and Y-maze tests, were performed on T. gondii-infected and uninfected Tg2576 mice. Results revealed that whereas the level of IFN-γ was unchanged, the levels of anti-inflammatory cytokines were significantly higher in T. gondii-infected mice than in uninfected mice, and in BV-2 cells treated with T. gondii lysate antigen. Furthermore, nitrite production from primary cultured brain microglial cells and BV-2 cells was reduced by the addition of T. gondii lysate antigen (TLA), and β-amyloid plaque deposition in the cortex and hippocampus of Tg2576 mouse brains was remarkably lower in T. gondii-infected AD mice than in uninfected controls. In addition, water maze and Y-maze test results revealed retarded cognitive capacities in uninfected mice as compared with infected mice. These findings demonstrate the favorable effects of the immunosuppression induced by T. gondii infection on the pathogenesis and progression of AD in Tg2576 mice.
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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.