MITOCHONDRIAL DYSFUNCTION IN SCHIZOPHRENIA

 

MITOCHONDRIAL

DYSFUNCTION IN SCHIZOPHRENIA: EVIDENCE FOR OXIDATIVE STRESS AND ABNORMAL GROWTH

FACTOR SUPPORT

 

Sabine

Bahn and colleagues

 

Babraham

Institute and Department of Psychiatry, University of Cambridge, UK

Stanley

Labs, Bethesda and Johns Hopkins, Baltimore, USA

 

 

The

etiology and pathophysiology of schizophrenia remain unknown.  A parallel

transcriptomics, proteomics and metabolomics approach was employed on human

brain tissue to explore the molecular disease signatures.  Results from this

integrative study showed that pathways associated with mitochondrial function

and oxidative stress, were most prominently altered.  White matter is

particularly vulnerable to free radical damage and schizophrenia white matter

showed the most prominent metabolite changes.  Cluster analysis of

transcriptional alterations, showed that genes related to energy metabolism and

oxidative stress differentiated almost 90% of schizophrenia patients from

controls (n=92), whilst confounding drug effects could be ruled out.  This

insight suggests a new concept for schizophrenia and may influence the approach

to treatment, diagnosis and disease prevention of schizophrenia and related

syndromes.

 

S.B. et al gratefully

acknowledge centre support through the Stanley Medical Research Institute