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dc.contributor.authorLow, Intanen_US
dc.contributor.authorKuo, Po-Chihen_US
dc.contributor.authorTsai, Cheng-Linen_US
dc.contributor.authorLiu, Yu-Hsiangen_US
dc.contributor.authorLin, Ming-Weien_US
dc.contributor.authorChao, Hsiang-Taien_US
dc.contributor.authorChen, Yong-Shengen_US
dc.contributor.authorHsieh, Jen-Chuenen_US
dc.contributor.authorChen, Li-Fenen_US
dc.date.accessioned2019-04-02T05:59:10Z-
dc.date.available2019-04-02T05:59:10Z-
dc.date.issued2018-11-20en_US
dc.identifier.issn1662-453Xen_US
dc.identifier.urihttp://dx.doi.org/10.3389/fnins.2018.00826en_US
dc.identifier.urihttp://hdl.handle.net/11536/148486-
dc.description.abstractThe irregularity and uncertainty of neurophysiologic signals across different time scales can be regarded as neural complexity, which is related to the adaptability of the nervous system and the information processing between neurons. We recently reported general loss of brain complexity, as measured by multiscale sample entropy (MSE), at pain-related regions in females with primary dysmenorrhea (PDM). However, it is unclear whether this loss of brain complexity is associated with inter-subject genetic variations. Brain-derived neurotrophic factor (BDNF) is a widely expressed neurotrophin in the brain and is crucial to neural plasticity. The BDNF Val66Met single-nucleotide polymorphism (SNP) is associated with mood, stress, and pain conditions. Therefore, we aimed to examine the interactions of BDNF Val66Met polymorphism and long-term menstrual pain experience on brain complexity. We genotyped BDNF Val66Met SNP in 80 PDM females (20 Val/Val, 31 Val/Met, 29 Met/Met) and 76 healthy female controls (25 Val/Val, 36 Val/Met, 15 Met/Met). MSE analysis was applied to neural source activity estimated from resting-state magnetoencephalography (MEG) signals during pain-free state. We found that brain complexity alterations were associated with the interactions of BDNF Val66Met polymorphism and menstrual pain experience. In healthy female controls, Met carriers (Val/Met and Met/Met) demonstrated lower brain complexity than Val/Val homozygotes in extensive brain regions, suggesting a possible protective role of Val/Val homozygosity in brain complexity. However, after experiencing long-term menstrual pain, the complexity differences between different genotypes in healthy controls were greatly diminished in PDM females, especially in the limbic system, including the hippocampus and amygdala. Our results suggest that pain experience preponderantly affects the effect of BDNF Val66Met polymorphism on brain complexity. The results of the present study also highlight the potential utilization of resting-state brain complexity for the development of new therapeutic strategies in patients with chronic pain.en_US
dc.language.isoen_USen_US
dc.subjectBDNF Val66Met polymorphismen_US
dc.subjectprimary dysmenorrheaen_US
dc.subjectbrain complexityen_US
dc.subjectmultiscale entropyen_US
dc.subjectmagnetoencephalographyen_US
dc.subjectchronic painen_US
dc.titleInteractions of BDNF Val66Met Polymorphism and Menstrual Pain on Brain Complexityen_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fnins.2018.00826en_US
dc.identifier.journalFRONTIERS IN NEUROSCIENCEen_US
dc.citation.volume12en_US
dc.contributor.department交大名義發表zh_TW
dc.contributor.department資訊工程學系zh_TW
dc.contributor.departmentNational Chiao Tung Universityen_US
dc.contributor.departmentDepartment of Computer Scienceen_US
dc.identifier.wosnumberWOS:000450694600001en_US
dc.citation.woscount0en_US
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