An examination of TOR1A variants in recurrent major depression.

F Heining, B Langguth, P Eichhammer, Domani M, Hajak G, P G Sand

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Article in International journal of molecular epidemiology and genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

F HeiningDepartment of Psychiatry, University of Regensburg Germany.

B Langguth

P Eichhammer

Domani M

Hajak G

P G Sand

University of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObservations of comorbid depression in subjects with primary dystonia have suggested a dual role for the TOR1A gene in mood disorders and movement disorders. We conducted a systematic search for carriers of the ΔGAG deletion and for other variants in TOR1A exon 5 among 414 Caucasian subjects with recurrent major depression from the Upper Palatinate.

findingsAllele frequencies were determined for 27 TOR1A diallelic markers, including two novel synonymous substitutions (L262L and E310E) in the region encoding the torsinA C-terminus, plus four novel variants in the gene's 3'UTR. No carriers of the ΔGAG deletion were observed. When data were compared to previously examined control populations, no significant allelic associations were noted after corrections for multiple testing.

conclusionsThe present study adds to the spectrum of TOR1A mutations but provides no evidence of a common genetic predisposition to DYT1 dystonia and recurrent major depression.

Indexed as

DYT1genetic variationrecurrent major depressionTOR1Atorsion dystonia

Identifiers

PMID22493756

PMCPMC3316444

OpenAlexW1594495103

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