Toxoplasma gondii as a Risk Factor for Early-Onset Schizophrenia: Analysis of Filter Paper Blood Samples Obtained at Birth

Mortensen, Preben Bo; Nørgaard‐Pedersen, Bent; Waltoft, Berit Lindum; Sørensen, Thomas Lund; Hougaard, David M.; Torrey, E. Fuller; Yolken, Robert H.

doi:10.1016/j.biopsych.2006.05.024

Cited by 242 publications

(163 citation statements)

References 21 publications

Supporting

Mentioning

154

Contrasting

Unclassified

Order By: Relevance

“…Inflammation, particularly of a low-grade nature, is a consistent pathological finding in schizophrenia [80][81][82], and as described earlier, some of this inflammation is associated with the GI tract [13]. Interestingly, T. gondii exposure is a well-documented risk factor for schizophrenia [83,84], and as a gut pathogen is a tool used in experimental models to produce an inflammatory state in the GI tract. Thus not surprisingly, T. gondii infection can drive the dysbiosis of resident microbial communities and bring about a state of increased GI permeability [85][86][87][88].…”

Section: Epithelial and Endothelial Barrier Integritiesmentioning

confidence: 58%

Gastroenterology issues in schizophrenia: Why the gut matters

Severance

2016

Eur. psychiatr.

View full text Add to dashboard Cite

Genetic and environmental studies implicate immune pathologies in schizophrenia. The body's largest immune organ is the gastrointestinal (GI) tract. Historical associations of GI conditions with mental illnesses predate the introduction of antipsychotics. Current studies of antipsychoticnaïve patients support that gut dysfunction may be inherent to the schizophrenia disease process. Risk factors for schizophrenia (inflammation, food intolerances, Toxoplasma gondii exposure, cellular barrier defects) are part of biological pathways that intersect those operant in the gut. Central to GI function is a homeostatic microbial community that early reports show is disrupted in schizophrenia. Bioactive and toxic products derived from digestion and microbial dysbiosis activate adaptive and innate immunity. Complement C1q, a brain-active systemic immune component, interacts with gut-related schizophrenia risk factors in clinical and experimental animal models. With accumulating evidence supporting newly discovered gut-brain physiological pathways, treatments to ameliorate brain symptoms of schizophrenia should be supplemented with therapies to correct GI dysfunction.

show abstract

Section: Epithelial and Endothelial Barrier Integritiesmentioning

confidence: 58%

Gastroenterology issues in schizophrenia: Why the gut matters

Severance

2016

Eur. psychiatr.

View full text Add to dashboard Cite

show abstract

“…gondii can alter brain function and induce changes in the behavior of its intermediate hosts (Mortensen et al 2007;Kar and Misra 2004;Arling et al 2009). In male LongEvans rats, Latent Toxoplasma infection resulted to reduced the normal aversion to cat odor and converted it into a mild attraction (Vyas et al 2007).…”

Section: Discussionmentioning

confidence: 99%

“…administration of ghrelin or its direct microinjection into the hippocampus, amygdale, or dorsal raphe nucleus induced anxiety-like behaviors in certain rat strains in the elevated plus maze, open field test and step-down/inhibitory avoidance test (Carlini et al 2002(Carlini et al , 2004. Also, both intra-third cerebroventricular and intraperitoneal administration of ghrelin to mice decreased duration of time in and number of entries into the open arms of an elevated plus maze when assessed ten minutes after injection (Mortensen et al 2007). Finally, a recent study demonstrated that intracerebroventricularly administration of ghrelin to neonatal chicks in a dose-dependent manner increased the latency to ambulate but decreased ambulation activity in the Open Field test, indicating an anxiogenic effect (Carvajal et al 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies demonstrated that T. gondii can modify brain function and intermediate host's behavior (Hermes et al 2008;Vyas et al 2007;Kannan et al 2010), and also increase the chances of serious psychological disturbances such as schizophrenia and bipolar disorders in human (Pearce et al 2012;Mortensen et al 2007). In addition there is correlation between T. gondii infection and mood disorders.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Toxoplasma gondii infection on anxiety, depression and ghrelin level in male rats

et al. 2014

View full text Add to dashboard Cite

The aim of the present study was to determine the effects of Toxoplasma gondii (T. gondii) infection on anxiety, depression and ghrelin level in male rats. Twenty four male rats were assessed in two equal groups. T. gondii tachyzoite (ip) were injected in infected group and control group received (2 ml) physiological serum (ip). Elevated plus Maze and swimming tests were used to assess anxiety and depression in rats respectively. The ghrelin and T. gondii IgG serum levels were measured by enzyme immunoassay kits. The Student's t test and Pearson correlation coefficient were used. The ghrelin serum level was significantly lower in the infected rats than control (P = 0.03). There were no significant differences in the depression and anxiety behavior between two groups. However, here were no significant correlations between ghrelin level and anxiety or depression in rats. It seems that latent T. gondii infection decreases the ghrelin serum level but does not change anxiety and depression like behaviors.

show abstract

“…Several research groups from different countries have shown that there is an increase in antibodies against the zoonotic protozoan Toxoplasma gondii in individuals with schizophrenia compared to individuals without the disease in the same populations (Alvarado-Esquivel et al, 2006;Wang et al, 2006;Cetinkaya et al, 2007;Niebuhr et al, 2008). Researchers have also shown that children born to mothers with antibodies to T. gondii are at an increased risk of developing schizophrenia (Brown et al, 2005;Mortensen, Nørgaard-Pedersen, Waltoft, Sørensen, Hougaard et al, 2007;Mortensen, Nørgaard-Pedersen, Waltoft, Sørensen, Hougaard, Torrey, et al, 2007). One study demonstrated that patients with schizophrenia and positive for antibodies to T. gondii had a significantly increased risk of dying from natural causes compared to patients with schizophrenia and no antibodies to T. gondii (Dickerson et al, 2007).…”

mentioning

confidence: 99%