ArticleASN neuro
Dissecting Amyloid Beta Deposition Using Distinct Strains of the Neurotropic Parasite Toxoplasma gondii as a Novel Tool.
Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- 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
- Beyond Latency: ChronicBiomedicines · 2025Review
- No evidence of Alzheimer's disease pathology in mice infected with Toxocara canis.Parasite (Paris, France) · 2025Article
- Toxoplasma gondii Infection of Alzheimer's Disease Mice Reduces Brain Amyloid Density Globally and Regionally.The Journal of infectious diseases · 2024Article
- 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
- High-throughput identification of Toxoplasma gondii effector proteins that target host cell transcription.Cell host & microbe · 2023Article
- The aging of the immune system and its implications for transplantation.GeroScience · 2023Review
- Infectious origin of Alzheimer's disease: Amyloid beta as a component of brain antimicrobial immunity.PLoS pathogens · 2022Review
- IFN-γ stimulated murine and human neurons mount anti-parasitic defenses against the intracellular parasite Toxoplasma gondii.Nature communications · 2022Article
- Low cerebrospinal fluid Amyloid-βeta 1-42 in patients with tuberculous meningitis.BMC neurology · 2021Article
- 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
- Can quantifying morphology and TMEM119 expression distinguish between microglia and infiltrating macrophages after ischemic stroke and reperfusion in male and female mice?Journal of neuroinflammation · 2021Article
- Pathophysiological Mechanisms of Cognitive Impairment and Neurodegeneration byBrain sciences · 2020Review
- Aging with Toxoplasma gondii results in pathogen clearance, resolution of inflammation, and minimal consequences to learning and memory.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Genetic and pathologic data suggest that amyloid beta (Aβ), produced by processing of the amyloid precursor protein, is a major initiator of Alzheimer's disease (AD). To gain new insights into Aβ modulation, we sought to harness the power of the coevolution between the neurotropic parasite Toxoplasma gondii and the mammalian brain. Two prior studies attributed Toxoplasma-associated protection against Aβ to increases in anti-inflammatory cytokines (TGF-β and IL-10) and infiltrating phagocytic monocytes. These studies only used one Toxoplasma strain making it difficult to determine if the noted changes were associated with Aβ protection or simply infection. To address this limitation, we infected a third human amyloid precursor protein AD mouse model (J20) with each of the genetically distinct, canonical strains of Toxoplasma (Type I, Type II, or Type III). We then evaluated the central nervous system (CNS) for Aβ deposition, immune cell responses, global cytokine environment, and parasite burden. We found that only Type II infection was protective against Aβ deposition despite both Type II and Type III strains establishing a chronic CNS infection and inflammatory response. Compared with uninfected and Type I-infected mice, both Type II- and Type III-infected mice showed increased numbers of CNS T cells and microglia and elevated pro-inflammatory cytokines, but neither group showed a >2-fold elevation of TGF-β or IL-10. These data suggest that we can now use our identification of protective (Type II) and nonprotective (Type III) Toxoplasma strains to determine what parasite and host factors are linked to decreased Aβ burden rather than simply with infection.
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