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Psychiatric Genetics:
doi: 10.1097/YPG.0b013e328358642f
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Analysis of Stathmin gene variation in patients with panic disorder and agoraphobia

Bräuer, Davida; Görgens, Heikec; Einsle, Franziskaa; Zimmermann, Katrind; Noack, Barbarae; von Kannen, Stephaniec; Hoyer, Jürgena; Strobel, Alexanderb; Weidner, Kerstind; Jatzwauk, Mariac; Ziegler, Andreasf; Hemmelmann, Claudiaf; Köllner, Volkerg,h; Schackert, Hans K.c

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Author Information

aInstitute of Clinical Psychology and Psychotherapy

bInstitute of Psychology II, Technische Universitaet Dresden

Departments of cSurgical Research

dPsychotherapy and Psychosomatic Medicine

ePeriodontology, University Hospital Carl Gustav Carus, Technische Universitaet Dresden, Dresden

fInstitute of Medical Biometry and Statistics, University Hospital Schleswig-Holstein, Campus Lübeck, University of Lübeck, Lübeck

gClinic of Psychosomatic Medicine, Mediclin-Bliestal Clinics, Blieskastel

hFaculty of Medicine, Saarland University, Homburg, Germany

David Bräuer and Heike Görgens contributed equally to the writing of this article.

Correspondence to David Bräuer, Diploma-Psychology, Institute of Clinical Psychology and Psychotherapy, Technische Universitaet Dresden, Hohe Strasse 53, 01187 Dresden, Germany Tel: +49 351 463 36954; fax: +49 351 463 36955; e-mail: braeuer@psychologie.tu-dresden.de

Received May 22, 2012

Accepted June 27, 2012

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Summary

A comprehensive understanding of the development and maintenance of fear-related disorders such as agoraphobia should take genetic mechanisms into account, which impact on the neural circuitry involved in fear conditioning.

In a knockout study of mice carried out by Shumyatsky et al. (2005), Stathmin, an inhibitor of microtubule formation, was attributed an essential function in the regulation of neural circuitry involved in fear conditioning. An analogous role of Stathmin in humans has been suggested by Brocke et al. (2010), who found associations of Stathmin gene variation and fear-related endophenotypes. Furthermore, Ehlis et al. (2011) observed Stathmin gene variants to be associated with cognitive-affective processing. On the basis of these findings, we examined whether variants of the Stathmin gene are associated with agoraphobia in humans.

Mental disorders were assessed by the Munich-Composite International Diagnostic Interview (Wittchen and Pfister, 1996) in 95 patients with agoraphobia (PA) and 119 healthy controls (HC). A complete sequence analysis of coding and adjacent intronic regions of Stathmin was carried out in all participants.

There were no significant differences in the genotypic frequencies of 15 Stathmin polymorphisms between PA and HC (all P>0.05). Allele frequencies of c.−2045C>T were n=94/1/0 in PA and n=118/1/0 in the HC group, for c.−2036C>T frequencies were n=95/0/0 in the PA group, and n=117/2/0 in the HC group. The frequencies for c.−90_−91delAG located in exon 1 were n=94/1/0 in the PA group and 118/1/0 in the HC group. The frequencies for the variants located in intron 1 region were n=95/0/0 in the PA group and n=118/1/0 in the HC group for c.−63+236A>G, n=94/1/0 in the PA group and n=119/0/0 in the HC group for c.−63+438C>T, and n=24/42/29 in the PA group and n=20/64/35 in the HC group for c.−63+524G>T (rs213641). Allele frequencies for c.−63+689C>T were n=91/4/0 in the PA group and n=114/5/0 in the HC group, for c.−62–810C>A frequencies were n=95/0/0 in the PA group and n=118/1/0 in the HC group, and for c.−62–122dupA frequencies were n=94/1/0 in the PA group and n=119/0/0 in the HC group. Frequencies for c.187–5dupT located in intron 3 were n=94/1/0 in the PA group and n=119/0/0 in the HC group. The frequencies for the variants located in intron 4 were n=93/2/0 in the PA group and n=110/9/0 in the HC group for c.378+11T>C, n=95/0/0 in the PA group and n=118/1/0 in the HC group for c.378+209_213delTGTTA, n=95/0/0 in the PA group and n=118/1/0 in the HC group for c.378+216_219delTTCT, n=93/2/0 in the PA group and n=119/0/0 in the HC group for c. *360A>G, and n=94/1/0 in the PA group and 119/0/0 in the HC group for c. *564_567dupGACC.

For Stathmin, allele frequencies between women and men were not significantly different for all single nucleotide polymorphisms (all P>0.05).

Our results do not argue for a major role of Stathmin variants in agoraphobia. However, further research is required to evaluate the potential impact of deleterious Stathmin mutations on more severe forms of agoraphobia, as our cases predominantly had mild forms of the disorder.

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Acknowledgements
Conflicts of interest

There are no conflicts of interest.

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References

Brocke B, Lesch KP, Armbruster D, Moser DA, Müller A, Strobel A, et al. Stathmin, a gene regulating neural plasticity, affects fear and anxiety processing in humans. Am J Med Genet B Neuropsychiatr Genet. 2010;153B:243–251

Ehlis AC, Bauernschmitt K, Dresler T, Hahn T, Herrmann MJ, Röser C, et al. Influence of a genetic variant of the neuronal growth associated protein Stathmin 1 on cognitive and affective control processes: an event-related potential study. Am J Med Genet B Neuropsychiatr. 2011;156B:291–302

Shumyatsky GP, Malleret G, Shin R-M, Takizawa S, Tully K, Tsvetkov E, et al. Stathmin, a gene enriched in the amygdale, controls both learned and innate fear. Cell. 2005;123:697–709

Wittchen H-U, Pfister H DIA-X. Composite International Diagnostic Interview for ICD 10 and DSM-IV. 1996 Frankfurt Swets & Zeitlinger

© 2013 Lippincott Williams & Wilkins, Inc.

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