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Prolidase levels are higher in patients with bipolar disorder than in those without the condition, and could serve as a trait marker in bipolar disorder diagnosis, say Turkish researchers.
Prolidase - a proline splitting enzyme - is thought to play a role in oxidative metabolism, which has been found to be impaired in patients with bipolar disorder, explain Salih Selek (Harran University, Sanliurfa) and colleagues.
This, say the researchers, “lends support to the hypothesis that oxidative stress may contribute to the pathophysiology of bipolar disorder.”
To investigate prolidase activity in patients with bipolar disorder, and assess its effectiveness as a diagnostic marker, the team studied 66 patients with bipolar I disorder (31 women) and 66 mentally healthy controls (31 women) who were aged a mean of 32 and 30 years, respectively.
Of the patients with bipolar disorder, 22 were manic, 20 were depressive, and 24 were euthymic.
Blood samples were collected from all of the participants and tested for prolidase activity using a specific assay.
The researchers found that prolidase levels were significantly higher in bipolar disorder patients than controls, at 534.58 versus 415.61 U/l, respectively.
However, there were no significant differences in prolidase levels among manic, depressive, and euthymic bipolar disorder patients, at 532.05, 538.96, and 532.66 U/l, respectively.
Receiver-operating characteristic curve analysis revealed that a prolidase level cutoff point of 502.94 U/l had a positive and negative predictive value for bipolar disorder of 98.5% and 92.4%, respectively.
Selek and team conclude in the Journal of Affective Disorders: “Prolidase activity is impaired in bipolar disorder, which may be associated with oxidative stress.”
They add: “Prolidase activity may be a trait marker for diagnosing bipolar disorder.”
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010
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1A binding reductions in euthymic bipolar disorder patients]]>
Posted by admin on July 25th, 2010
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5-HT1A receptor binding is not reduced in medicated euthymic bipolar disorder patients versus healthy individuals, say researchers in findings that contrast with the reductions seen in unipolar and bipolar depressed patients.
Previous studies of 5-HT1A receptor binding have focused on unipolar and bipolar depressed patients, with mixed results, but the greatest reductions observed have been in patients with a family history of bipolar disorder.
To examine binding reductions in euthymic bipolar disorder patients, Peter Sargent, from Warneford Hospital in Oxford, UK, and colleagues performed positron emission tomography using the selective 5-HT1A receptor ligand [carbonyl-11C]WAY-100635 in eight medicated euthymic bipolar disorder patients and eight healthy controls.
Although the team found a significant negative correlation between age and global postsynaptic parametric binding potential, there was no significant difference in binding potential between patients and controls, at averages of 4.24 and 4.34, respectively.
The results, published in the Journal of Affective Disorders, also demonstrated no significant differences in regional parametric binding potentials between the groups. There was no significant correlation between global binding potentials and depression scores in patients.
The team concludes: “Longitudinal studies examining 5-HT1A binding in both medicated and unmedicated patients with bipolar disorder are warranted to clarify whether there may be effects of medication on 5-HT1A binding or whether there is an effect of mood state in bipolar disorder with normalization of 5-HT1A binding in the euthymic state.”
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009
Variations in the D-amino acid oxidase activator gene (DAOA) are linked to the development of bipolar disorder and schizophrenia, although they account for only a part of genetic susceptibility, UK study findings suggest.
Previous studies have associated the DAOA/G30 locus or the neighboring region of chromosome 13q33.2 with both bipolar disorder and schizophrenia, while four single nucleotide polymorphisms (SNPs) at 12q24.11 have been linked to schizophrenia. However, the results have been conflicting.
Hugh Gurling, from University College London, and colleagues therefore genotyped 431 schizophrenia patients, 303 bipolar disorder patients, and 442 ancestrally matched controls with no history of mental disorder.
All participants were genotyped for 11 SNPs at the DAOA locus, with schizophrenia patients and controls also genotyped for three SNPs at the D-amino acid oxidase gene (DAO) locus on chromosome 12.
The results, published in the journal Behavioral and Brain Functions, reveal that the SNP rs3918342 (M23) at the DAOA locus was significantly associated with schizophrenia, bipolar disorder, and both conditions combined.
There was a trend toward association with schizophrenia for the SNPs rs3916967 (M14) and rs1421292 (M24), with the latter also marginally significantly associated with both conditions combined.
The team also found that there was a haplotypic association with schizophrenia for the markers rs778293 (M22), rs3918342 (M23), and rs1421292 (M42), with alleles G, T, A increasing the risk for schizophrenia at an estimated frequency of 1.8% in controls and 3.6% in patients. None of the three DOA SNPs were associated with schizophrenia.
The team concludes: “Our findings point to a role for DAOA in both schizophrenia and bipolar disorder. However, it is evident that this locus can account for only a small proportion of genetic susceptibility to these disorders.”
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009
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