Toxoplasma gondii Infection in the Brain Inhibits Neuronal Degeneration and Learning and Memory Impairments in a Murine Model of Alzheimer's Disease

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.

Characterizing Gene and Protein Crosstalks in Subjects at Risk of Developing Alzheimer’s Disease: A New Computational Approach

“…Similarly, the enrichment of metabolic pathways, organismal systems including nervous and immune system pathways, and common signaling pathways of the environmental information processing category is also expected and well-supported in the literature [54][55][56][57][58][59][60][61][62][63][64][65][66][67][68]. Interestingly, several genetic information processing pathways, including cell cycle regulation and DNA replication and repair, were found to be enriched.…”

Latent Toxoplasmosis gondii: Emerging Evidence for Influences on Neuropsychiatric Disorders

“…Efforts to examine this linkage have been undertaken in a rodent model, using mice bred to carry the rodent equivalent of AD, with and without T. gondii infection. 52 Mice infected with T. gondii had significantly lower rates of b-amyloid plaque formation in cortex and hippocampus, and maintained learning and memory skills that declined in the T. gondii seronegative group. The authors felt that these results were due to the increased presence of some antiinflammatory processes in the seropositive group.…”

Is there any role of latent toxoplasmosis in schizophrenia disease?

“…6,7 After ingestion, sporozoites and bradyzoites released from oocysts and cysts invade intestinal cells and are converted to tachyzoites. 8 Conflicts of interest: The authors declare that there are no conflicts of interest related to the subject matter or materials discussed in this article.…”