Mitochondrial dysfunction in schizophrenia: evidence for compromised brain metabolism and oxidative stress
S Prabakaran, J E Swatton, M M Ryan, S J Huffaker, JT-J Huang, J L Griffin, M Wayland, T Freeman, F Dudbridge, K S Lilley, N A Karp, S Hester, D Tkachev, M L Mimmack, R H Yolken, M J Webster, E F Torrey and S Bahn
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. Almost half the altered proteins identified by proteomics were associated with mitochondrial function and oxidative stress responses. This was mirrored by transcriptional and metabolite perturbations. Cluster analysis of transcriptional alterations showed that genes related to energy metabolism and oxidative stress differentiated almost 90% of schizophrenia patients from controls, while confounding drug effects could be ruled out. We propose that oxidative stress and the ensuing cellular adaptations are linked to the schizophrenia disease process and hope that this new disease concept may advance the approach to treatment, diagnosis and disease prevention of schizophrenia and related syndromes. Molecular Psychiatry (2004) 9, 684-697. Published online 20 April 2004.
Friday, October 01, 2004
A Cause of Schizophrenia?
Here's the abstract for a paper presenting some interesting new research on the causes of schizophrenia. Apparently it may be caused by damage to mitochondria which leads to problems in their functioning. The damage may, in turn, may in part be the result of genetic predispositions.