The neuropathology linking T. gondii infection and schizophrenia?

A quote to begin: "findings suggest that T gondii [Toxoplasma gondii] infection causes substantial and widespread immune activation indicative of neural damage and reactive tissue repair in the animal model that partly overlaps with changes observed in the brains of schizophrenia patients."

So said the very interesting paper by Jakub Tomasik and colleagues [1] who set about comparing results from a mouse model of "chronic T gondii infection" looking for serum and brain signatures with those in postmortem "brain samples from 35 schizophrenia patients and 33 healthy controls." Researchers found that mice infected with T. gondii were pretty 'immune-stimulated' as a result; also manifesting with "neural damage and reactive tissue repair". Some of these immune consequences also seemingly 'overlapped' with what was observed in the very precious brain samples from those previously diagnosed with schizophrenia, particularly when it came to "C-reactive protein (CRP), interleukin-1 beta (IL-1β), interferon gamma (IFNγ), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular cell adhesion molecule 1 (VCAM-1)." The authors conclude that any shared pathophysiology might be "a key step towards understanding their specific contributions to pathogenesis."

I'd like to think that the Tomasik paper is an important next step in the whole idea that T. gondii infection might show some important links with at least some schizophrenia (see here). Still a point of discussion in some quarters [2] insofar as the hows and whys of any association (see here), there is nevertheless, some quite reliable research appearing in the peer-reviewed domain to suggest that there may a link, correlation if you will, between this parasitic protozoan and the appearance of some schizophrenia or schizophrenia-linked symptoms. Putting some scientific flesh on the bones of 'mechanisms' through which infection might link to schizophrenia is important.

That being said, I do think we have to be slightly cautious when it comes to changes in immune function in relation to schizophrenia being solely pinned down to T. gondii infection. Given for example, the growing significance of something like CRP to schizophrenia in general (see here), I think you would be hard-pressed to say this is all down to T. gondii infection. Indeed, the maternal immune activation hypothesis may well play a role here (see here) as might the wider implications of something like inflammation when it comes to the wider arena of psychiatry (see here).

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[1] Tomasik J. et al. Shared Immune and Repair Markers During Experimental Toxoplasma Chronic Brain Infection and Schizophrenia. Schizophr Bull. 2015 Sep 20. pii: sbv134.

[2] Wolf PJ. & Hamilton FE. Flawed analyses undermine proposed relationship between childhood cat ownership and schizophrenia. Schizophr Res. 2015 Aug 14. pii: S0920-9964(15)00427-2.

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Tomasik J, Schultz TL, Kluge W, Yolken RH, Bahn S, & Carruthers VB (2015). Shared Immune and Repair Markers During Experimental Toxoplasma Chronic Brain Infection and Schizophrenia. Schizophrenia bulletin PMID: 26392628