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Toxoplasma gondii & Human Phenotype

Compendium of Known Effects and Ongoing Research

prefrontal cortex

Cerebral complement C1q activation in chronic Toxoplasma infection

May 24, 2016
Xiao, J.C., Li, Y., Gressitt, K.L., He, H., Kannan, G., Schultz, T.L., Svezhova, N., Carruthers, V.B., Pletnikov, M.V., Yolken, R.H., Severance, E.G.
Brain Behav. Immun. 2016; 58: 52-56
Click for abstract
Exposure to the neurotropic parasite, Toxoplasma gondii, causes significant brain and behavioral anomalies in humans and other mammals. Understanding the cellular mechanisms of T. gondii-generated brain pathologies would aid the advancement of novel strategies to reduce disease. Complement factor C1 q is part of a classic immune pathway that functions peripherally to tag and remove infectious agents and cellular debris from circulation. In the developing and adult brain, C1 q modifies neuronal architecture through synapse marking and pruning. T. gondii exposure and complement activation have both been implicated in the development of complex brain disorders such as schizophrenia. Thus, it seems logical that mechanistically, the physiological pathways associated with these two factors are connected. We employed a rodent model of chronic infection to investigate the extent to which cyst presence in the brain triggers activation of cerebral C1 q. Compared to uninfected mice, cortical C1 q was highly expressed at both the RNA and protein levels in infected animals bearing a high cyst burden. In these mice, C1 q protein localized to cytoplasm, adjacent to GFAP-labeled astrocytes, near degenerating cysts, and in punctate patterns along processes. In summary, our results demonstrated an upregulation of cerebral C1q in response to latent T. gondii infection. Our data preliminarily suggest that this complement activity may aid in the clearance of this parasite from the CNS and in so doing, have consequences for the connectivity of neighboring cells and synapses.

Tagged: glia, MAG1 antibodies, neurons, prefrontal cortex, psychiatry, toxoplasmosis

Mental health

Schizophrenia susceptibility genes directly implicated in the life cycles of pathogens: Cytomegalovirus, influenza, herpes simplex, rubella, and Toxoplasma gondii.

October 30, 2006
Carter CJ.
Schizophrenia Bulletin 2006; 35: 1163-1182
Click for abstract
Over 130 genes have been associated with schizophrenia in genetic studies. None of these has reached a sufficient level of confidence to be accepted as a universal susceptibility gene and problems of replicability suggest that many may be false positives. Nevertheless, these genes can be grouped into distinct families related to glutamate transmission (in particular related to NMDA receptor function), the control of synaptic plasticity, dopaminergic transmission, oxidative stress, glutathione and quinone metabolism and oligodendrocyte viability. These families mirror the processes disrupted in the schizophrenic brain and certain gene families can be linked together to form a clearly defined signalling cascade involved in the phenomenon of NMDA receptor-dependent long-term potentiation and synaptic plasticity, that may be interconnected with oligodendrocyte and oxidative stress-related pathways. Many of the protein products of these genes interact with each other, forming complex integrated networks. Certain high-interest genes (for example DISC1, NRG1, COMT) may exert multiple effects on different areas of these pathways, while others exert more specific effects on certain branches. The convergence of a large number of genes on a definable signaling network raises the possibility of numerous interactions between gene candidates, and suggests that a targeted multigenic pathway approach would be useful in gene association studies. (c) 2006 Elsevier B.V. All rights reserved.

Tagged: association, catechol-o-methyltransferase, cell-death, cortical pyramidal neurons, dendritic spine density, DNA microarray, Dopamine, gene, glutathione, influenza hemagglutinin peptide, multigenic, nitric-oxide synthase, nmda, nmda receptor, oligodendrocyte, oxidative stress, polymorphism, prefrontal cortex, quinone, Schizophrenia, synaptic plasticity

Mental health

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