POSTER

POSTER

 

 

MITOCHONDRIAL

DYSFUNCTION IN SCHIZOPHRENIA: OXIDATIVE STRESSING

 

S.

Huffamer1,2, M. Ryan1,2, and S. Bahn1,2

1Department of

Neurobiology, Babraham Institute, Cambridge CB2 4AT, UK; 2Department

of Psychiatry, University of Cambridge, Addenbrooke’s Hospital, Cambridge CB2

1QQ, UK

 

 

 

The onset

and etiology of schizophrenia has been implicated with a wide range of genetic

and epigenetic factors with limited agreement of the true causality.  The

ambiguousness of the causative agents and the heterogeneity of behavioral

phenotypes have been suggested as evidence that schizophrenia is a “catch-all”

category describing many etiologically heterogeneous neuropsychiatric

abnormalities.

 

Using

Affymetrix microarray technology representing 22,000+ human transcripts, we have

generated a dataset from the prefrontal cortex of 106 well-matched unaffected

and schizophrenia patients.  We observed significant changes in transcripts

encoding genes involved in mitochondrial function and oxidative stress reaction

pathways in schizophrenia patients.  Converging proteomics and metabolomics

investigations imply that dysregulations of metabolic activity and increased

levels of reactive oxygen species may closely underlie the symptoms of

schizophrenia, despite the apparent heterogeneity of the disorder and its

causative factors

 

Our

findings point toward oxidative stress injury and perhaps microvasculature

abnormalities in patients suffering from schizophrenia and related syndromes. 

However, the specific underlying developmental, genetic, and epigenetic factors

remain elusive.

 

The

authors gratefully acknowledge support from the Stanley Medical Research

Institute and the NIH-Cambridge University Health Science Scholars Program.