Excess hydrogen sulfide and polysulfides production underlies a schizophrenia pathophysiology

Mice with the C3H background show greater behavioral propensity for schizophrenia, including lower prepulse inhibition (PPI), than C57BL/6 (B6) mice.



Very interesting paper.

Because H2S is distributed systemically, some somatic diseases are also affected by H2S. Ulcerative colitis is an inflammatory bowel disease, and H2S overproduction contributes to the etiology of this disease (Roediger et al , 1997). On the other hand, H2S is present in joints and acts as a proinflammatory mediator (Muniraj et al , 2017); therefore, rheumatic diseases might be associated with decreased production of H2S. Comorbidity has been reported between ulcerative colitis and schizophrenia (Cucino & Sonnenberg, 2001), whereas rheumatoid arthritis occurs at a relatively low frequency in schizophrenia patients (Leucht et al , 2007).

In schizophrenia, biomarkers are of cardinal importance for early intervention and improved prognoses (Morrison et al , 2012; Fusar‐Poli et al , 2013). Biomarkers can be also used to categorize patients and determine optimal therapeutics. Our postmortem study suggested a positive correlation between symptomatic severity and “sulfide stress”, and in living patients the present results highlight the potential benefit of examining MPST expression levels in scalp hair follicles. The use of scalp hair follicles is advantageous because of the convenience and noninvasiveness of sampling (Maekawa et al , 2015).

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How do we fix this?

I don’t know. I guess they will work on an inhibitor.

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