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Neurotropic Infectious Agents and Cognitive Impairment in Schizophrenia

Posted on 12 Nov 2012
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

 

 

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.