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Post-stroke fatigue may be associated with the promoter region of a monoamine oxidase a gene polymorphism

Cited 13 time in Web of Science Cited 15 time in Scopus
Authors

Choi-Kwon, Smi; Ko, Mihye; Jun, Sang-Eun; Kim, Juhan; Cho, Kyung-Hee; Nah, Hyun-Wook; Song, Hasup; Kim, Jong S.

Issue Date
2017-02
Publisher
S. Karger AG
Citation
Cerebrovascular Diseases, Vol.43 No.1-2, pp.54-58
Abstract
Background: Post-stroke fatigue (PSF) is a common sequela of stroke. Despite reports of serotonergic involvement in the etiology of PSF, the potential contribution of serotonergic genes in the development of PSF needs to be investigated. Methods: A total of 373 patients, who experienced ischemic stroke for PSF, were evaluated 3 months after the stroke. PSF was assessed using the Fatigue Severity Scale. The genomic DNA collected and stored in a -70 degrees C freezer was genotyped for 6 polymorphisms in genes associated with serotonin synthesis (tryptophan hydroxylase 1 (TPH1) A218C, TPH2 rs10879355, and TPH2 rs4641528), transport (the promoter region of the serotonin transporter protein), and catabolism (the 30-bp functional variable number tandem repeat) polymorphism in the promoter region of monoamine oxidase A (MAO-A). Results: Among the 373 patients, 164 (44%) had PSF. All patients were ethnic Koreans. Of the 6 polymorphisms examined, only one marker, that is, low-activity MAOA was associated with PSF (p < 0.05) in female patients. Multiple logistic regression analyses showed that post-stroke depression (PSD; 95% CI 1.561-14.323, p = 0.006) and low MAO-A activity (95% CI 0.166-0.722, p = 0.005) were factors associated with PSF in female patients, whereas only PSD (95% CI 5.511-65.269, p = 0.000) was associated with PSF in male patients. Conclusions: Our findings suggest that PSF may be associated with a genetic polymorphism involving MAO-A, at least in female stroke patients. (C) 2016 S. Karger AG, Basel
ISSN
1015-9770
Language
English
URI
https://hdl.handle.net/10371/138919
DOI
https://doi.org/10.1159/000450894
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