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Updated 14 November 2012 E-mail discussion
Printable version

Live Discussion: Neurotropic Infectious Agents and Cognitive Impairment in Schizophrenia


Vishwajit Nimgaonkar

Mikhail Pletnikov

Konasale Prasad

Robert Yolken

On Tuesday, 13 November 2012, SRF held another installment in our Schizophrenia Bulletin theme section Webinar series to learn about and discuss this topic.

Thanks to the Maryland Psychiatric Research Center and Oxford Press, publishers of Schizophrenia Bulletin, for kindly providing open access to the introductory article for this Webinar.

Listen to the Webinar


Vishwajit Nimgaonkar's Presentation


Mikhail Pletnikov's Presentation


Konasale Prasad's Presentation


Robert Yolken's Presentation

View Comments By:
Georg Winterer — Posted 30 October 2012
Chris Carter — Posted 4 November 2012


Background Text
by Michele Solis

Infectious agents like the human habitat well enough, and some even prefer our nervous systems. As researchers debate whether infections contribute to schizophrenia risk, some scientists are beginning to ask whether infectious agents can also alter mental processes in people already diagnosed with schizophrenia.

Robert Yolken of Johns Hopkins University provided an overview of this “epidiagnostic” idea, which sees the vagaries of infection as possible modulators of processes such as cognitive functions among patients.

Researchers are now specifically exploring whether the cognitive impairments in schizophrenia are modified by infections with herpes simplex virus 1 (HSV1) and the parasite Toxoplasma gondii. Konasale Prasad of the University of Pittsburgh described work on HSV1, which, once it infects a person, remains in the nervous system throughout life, alternating between dormant and active states. HSV1-exposed people with schizophrenia exhibit worse cognitive symptoms in the realms of working memory, verbal memory, and executive function compared with unexposed patients with schizophrenia. Preliminary experiments now suggest that treatment with anti-herpes medications can improve these impairments. Importantly, even people without schizophrenia perform less well on specific cognitive tasks if they have been exposed to HSV1. Because the integrity of the immune system could modulate vulnerability to infection in the first place, Vishwajit Nimgaonkar of the University of Pittsburgh discussed potential interactions between infection and host genetic variation at the major histocompatibility complex (MHC) locus, a region containing immune-related genes that has been implicated in schizophrenia. This has offered up a potential interaction between a common variant in the region and HSV1 exposure on schizophrenia risk, and further studies are needed.

Toxoplasma gondii, a notorious resident of cats' litter boxes, may instigate cognitive deficits in humans upon infecting their nervous systems. Animal models of T. gondii infection have been developed to study this process in detail, and Mikhail Pletnikov of Johns Hopkins University discussed work in rodents infected with the parasite. These show impairments in spatial learning and memory analogous to impairments found in schizophrenia. Exploring these diverse questions may open up some novel avenues for treatment of cognitive impairments and provide some insight into the epidemiological hints of roles for infection in schizophrenia.


Comments on Online Discussion
Comment by:  Georg Winterer (Disclosure)
Submitted 29 October 2012 Posted 30 October 2012

Great topic! Myself, I have recently started to think about the same issue, in particular, how to answer this question in a "quasi-experimental" setting (as part of a population-based cohort study) project in preparation.

View all comments by Georg Winterer


Comment by:  Chris Carter
Submitted 1 November 2012 Posted 4 November 2012

This Webinar group has made an enormous contribution regarding the roles of pathogens in schizophrenia and related disorders. Although pathogens have been implicated in most diseases, there has been a certain reluctance in accepting any causal relationship (despite odds ratios generally higher than those of most genes (Torrey et al., 2012; Arias et al., 2012). This is partly due to the high prevalence of infection, compared with the much lower incidence of disease. For example, Toxoplasmosis may infect 30 percent of the global population (Henriquez et al., 2009), versus a schizophrenia incidence of about 1 percent (Saha et al., 2005).

Genetic studies currently hold center stage and have yielded an enormous amount of useful information concerning the pathology of numerous disorders, although in the psychiatric field, this has not yet led to the development of radically new...  Read more


View all comments by Chris Carter
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