Department of Psychological Medicine, Christchurch Medical School, University of Otago, Terrace House, 4 Oxford Terrace, PO Box 4345, Christchurch, New Zealand, E-mail: paul.edgar@chmeds.ac.nz

SIR - The authors, Sanders and Gejman, suggest that major corrections are indicated for 'Comparative proteome analysis of the hippocampus implicates chromosome 6q in schizophrenia' on the basis that the functional gene location for DBI is on chromosome 2q rather than 6q. At the time of acceptance of the manuscript the OMIM database listed the functional DBI gene loci as '6q but inconsistent', see Table 2 of the paper. However, their correction does not affect the conclusions of the paper. In their own words '..we agree that their (Edgar et al) proteomic experiment points to 6q25.3-q26 as a chromosomal region with an increased likelihood of containing a gene involved in the etiology of schizophrenia...'. The other prime conclusion of the paper, which is not questioned, is that the proteins DBI, TCP-1, SOD-2 and CRMP are significantly altered in concentration in a set of post mortem schizophrenic hippocampi when compared to a control set.

A purpose of the authors is revealed in the final paragraph when they state 'the primary support for a schizophrenia susceptibility gene in 6q13-q26 remains linkage mapping results'. Results, to which the authors themselves have contributed. However, it is well known that linkage mapping results point to a plethora of possible susceptibility loci, on a multitude of chromosomes. Although proteomics, as they suggest, is in 'its infancy' our work is the first proteomic pointer towards a schizophrenia susceptibility loci. We suggest that a combination of proteomics and linkage mapping results together will prove helpful in identifying valid loci, one of which may be 6q25.3-q26.