A Parasitic Disease's Role in the Development of Psychiatric Disorders

Article

New research has discovered how the toxoplasmosis parasite may activate the development of schizophrenia and other bipolar disorders.

New research has discovered how the toxoplasmosis parasite may activate the development of schizophrenia and other bipolar disorders.

Members of Leed University’s Faculty of Biological Sciences found that the parasite may impact the production of dopamine, which plays a role in “mood, sociability, attention, motivation, and sleep patterns,” has a long-lived association with schizophrenia, and is the target of all current schizophrenia drugs. The parasite infects the brain by forming a cyst and producing tyrosine hydroxylase, which is necessary to produce dopamine.

“Toxoplasmosis changes some of the chemical messages in the brain, and these changes can have an enormous effect on behavior,” said Dr. Gleen McConkey, lead researcher of the project. “Studies have shown there is a direct statistical link between incidences of schizophrenia and toxoplasmosis infection and our study is the first step in discovering why there is this link.”

According to the researchers, toxoplasmosis is “relatively common,” impacting 10-20% of the UK population and about 20% of the US population, who are all estimated to carry the parasite as cysts.

“It’s highly unlikely that we will find one definitive trigger for schizophrenia as there are many factors involved,” said McConkey. “But our studies will provide a clue to how toxoplasmosis infection—which is more common than you might think–can impact on the development of the condition in some individuals.”

“In addition, the ability of the parasite to make dopamine implies a potential link with other neurological conditions such as Parkinson’s Disease, Tourette’s syndrome and attention deficit disorders,” he added. “We’d like to extend our research to look at this possibility more closely.”

Findings of the study were also published in the March 11 online edition of PLoS ONE.

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