Wengenroth1, J. Swatton1, N. Karp2, H.S. Lilley2,

and S. Bahn1,3

1Department of

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

of Biochemistry, Cambridge Centre for Proteomics, University of Cambridge,

Cambridge, CB2 1QW, UK; 3Department of Psychiatry, University of

Cambridge, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK




disorder, also known as manic depression, is a disruptive mental health problem

involving episodes of extreme mood swings.  So far, the underlying

neuropathology has essentially been derived from drug effects.  Although several

neurotransmitter systems have been implicated to play a role in the etiology,

the full understanding of the pathophysiology of this affective disorder remains



In our

study we compared the protein expression profile of 10 prefrontal cortex samples

(grey and white matter respectively) from patients with bipolar disorder to 10

matched control samples.  After subjecting the proteins to 2D-fluorescence

differential gel electrophoresis (2D DIGE) we quantified the proteins using

Biological Variation Analysis software (Amersham) and sequenced the peptides by

LC/ Q-TOF mass spectrometry.


Interestingly, we discovered a largely increased protein expression profile.  In

particular proteins involved in energy metabolism, the cytoskeleton, protein

trafficking and neurodevelopment are generally over-expressed in bipolar

disorder.  In comparison to the results of an analogous study on schizophrenia,

findings from this study highlight the similarities as well as the distinct

pathways underlying this disease.  Those results are likely to give a further

insight into the complex neuropathology of this disease.




This work was supported

through a centre grant by the Stanley Medical Research Institute