Alterations of prolyl endopeptidase activity in the plasma of children with autistic spectrum disorders

doi:10.1186/1471-244X-5-27

BMC Psychiatry

Volume 5

Viewing options:

Abstract
Full text
PDF (277KB)

Associated material:

Related literature:

Articles citing this article
on Google Scholar
on PubMed Central
Other articles by authors
on Google Scholar

Momeni N
Nordström BM
Horstmann V
Avarseji H
Sivberg BV

on PubMed

Momeni N
Nordström BM
Horstmann V
Avarseji H
Sivberg BV
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

Research article

Alterations of prolyl endopeptidase activity in the plasma of children with autistic spectrum disorders

Naghi Momeni¹ , Berit M Nordström¹ , Vibeke Horstmann¹ , Hassan Avarseji² and Bengt V Sivberg¹

¹Department of Health Sciences, Autism Research, Lund University, Lund, Sweden

²Department of Neurology, Golestan University of Medical Science, Gorgan, Iran

author email corresponding author email

BMC Psychiatry 2005, 5:27doi:10.1186/1471-244X-5-27


Published:	2 June 2005

Abstract

Background

Prolyl Endopeptidase (PEP, EC 3.4.21.26), a cytosolic endopeptidase, hydrolyses peptide bonds on the carboxyl side of proline residue in proteins with a relatively small molecular weight. It has been shown that altered PEP activity is associated with various psychological diseases such as schizophrenia, mania and depression. Autistic Spectrum Disorders (ASD) are neuropsychiatric and behavioural syndromes affecting social behaviours and communication development. They are classified as developmental disorders. The aim of this study was to examine the hypothesis that PEP activity is also associated with ASDs.

Methods

Fluorometric assay was used to measure PEP activity in EDTA plasma in children with ASD (n = 18) aged 4–12 years (mean ± SD: 7.9 ± 2.5). These results were then compared to PEP activity in a control group of non-ASD children (n = 15) aged 2–10 years (mean ± SD: 6.4 ± 2.2).

Results

An alteration in PEP activity was found in the children with ASD compared to the control group. There was much greater variation of PEP activity in the group of ASD children when compared to the controls (SD= 39.9 and SD 9.6, respectively). This variation was significant (p < 0.0005), although the mean level of PEP activity in the group of ASD children was slightly higher than in the control group (124.4 and 134.1, respectively).

Conclusion

Our preliminary finding suggests a role for PEP enzyme in the pathophysiology of autism but further research should be conducted to establish its role in the aetiology of psychiatric and neurological disorders, including autism and related spectrum disorders.