The Unit for Resarch in Schizophrenia (URS) has already achieved very promising results concerning some of the causes and mechanisms linked to the disease:

• Glutathione, an abundant molecule in human cells and a powerful antioxidant, essential for the elimination of toxic substances in the human body (produced in particular by the absorption of oxygen), was found to be insufficient in the brain of chronic patients. A deficiency of glutathione is likely to hinder the normal functioning of contacts between nervous cells and to lead to defects in certain neurons.
  
• Glutathione is normally kept in adequate quantity in the human organism through regulating mechanisms; the production of glutathione requires mainly a synthesizing enzyme called GCL; in individuals affected by schizophrenia, the genes of this enzyme show anomalies that inhibit its functioning, which prevents it from producing enough glutathione. Such anomalies, which concern at least a third of patients, thus represent one of the possible causes of the disease.
  
• These results have been confirmed in young patients during their first psychotic episode, which proves that the anomalies of the glutathione system are inherent to the pathology of schizophrenia and not caused by the evolution of the disease nor by its treatment.
  This finding paves the way for the development of a biomarker profile allowing an early diagnosis of schizophrenia.
  
• The study of experimental models (laboratory work on mice) shows that a lowered glutathione level leads to numerous anomalies of nervous cells and behaviour, very similar to those observed in patients - which proves that deficient glutathione could be responsible for the symptoms of the disease.  
  
  
  

  
  Glutathione molecule

• The study of a new drug, resulting from the URS research program and conducted in collaboration with an australian research team, led to very interesting results. The drug is called N-acetyl-cysteine (NAC) and provides a component essential to the synthesis of glutathione. Chronic patients (of a certain age) who received this substance in addition to presently available treatments have experienced an amelioration of their symptoms, in particular of those which are not improved through classic medication. No negative side effects were observed. 
  In addition to clinical ameliorations, it was also observed, by means of electroencephalography (EEG), that the exploiting of auditory information by the brain is improved - a change that no other medication tested to this day has ever produced. The EEG recordings have furthermore shown that NAC improves the neuronal synchronization at rest, which adds a further argument to the objectively positive effects of the treatment. This amelioration corresponds in particular to that of certain disorganization symptoms in patients.   

To sum up, the URS has identified a risk factor for schizophrenia and a substance liable to partly correct it in patients who have suffered a long time from the disease. 

Moreover, the URS team has worked out the theory - based on the results of its studies and on scientific literature - that an imbalance between oxidations and reductions in cells plays a key role in the development of schizophrenia (and possibly of other diseases such bipolar disorders and autism). 
This imbalance is caused by genetic and environmental factors and leads to negative consequences on the development of the brain. Genetic factors can involve the metabolism of glutathione or other systems. Environmental factors can be manifold and of physical (complications at birth, infections, viruses, drug addiction, etc.) or psychological origin (traumas, stress, abuse, grief, etc.).
The result is an "oxidative stress" which will hinder the normal development of certain neurons and their connections in the brain.

Experimental evidence (on animals or cell cultures) shows that an imbalance between oxidations and reductions leads to consequences very similar to the anomalies observed in patients. Oxidation reduces in particular the activation of the "NMDA-R" receptor, essential to all learning and memory functions; this disturbs neuronal circuits which should normally be activated during cognitive performance.
Oxidative stress causes specific anomalies of a type of neurons that are crucial for the synchronization of large neuron populations directly involved in cognitive functions - an observation which brings up one of the key problems of the pathology of schizophrenia.

In brief, the imbalance between oxidations and reductions leading to an oxidative stress during brain development is likely to further the outbreak of schizophrenia.