Neuroendocrine Mechanisms Underlying Perimenopausal Risk for Trauma-Related Hyperarousal in Black Women
Neuroendocrine Mechanisms Underlying Perimenopausal Risk for Trauma-Related Hyperarousal in Black Women
批准号:
10618836
负责人:
Vasiliki Michopoulos
金额:
$75.27万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2022
资助国家:
美国
项目状态:
未结题
起止时间:
2022-05-06 至 2027-02-28
关键词:
AccelerationAcuteAddressAgeAmygdaloid structureBiological FactorsBlack raceBloodBrain regionClinicalDataDevelopmentEpigenetic ProcessEstradiolExtinctionFaceFemaleFrightFunctional Magnetic Resonance ImagingGoalsGonadotropinsHormonalHormonal ChangeHospitalsHypersensitivityInterviewKnowledgeLinkLongevityMental HealthNeurobiologyNeuroendocrinologyNeurosecretory SystemsOutcomeOvarian Steroid HormonePerimenopausePopulationPositioning AttributePost-Traumatic Stress DisordersPrefrontal CortexPremenopausePrevalenceProcessPsychopathologyPsychophysiologyResearchRiskStimulusStructureSymptomsTestingTimeTraumaUrban CommunityVariantWomanWorkanxiety symptomsblack womenconditioned feardepressive symptomsexperiencelow socioeconomic statusmood symptommortalitymortality riskneuroimagingpsychologicrecruitreproductiveresponsesexsocioeconomicssteroid hormonesymptom treatmenttrauma exposure
中文摘要
总结
英文摘要
Summary
The cumulative rate of repeated trauma exposure is greater in Black communities of urban, low socioeconomic
status and is associated with increased prevalence of adverse, posttraumatic mental health outcomes,
including posttraumatic stress disorder (PTSD). PTSD is associated with trauma-related hyperarousal (TRH)
and dysregulated fear responses that are dependent upon brain regions that modulate responses to threat,
including the amygdala and the ventromedial prefrontal cortex. One biological factor that confers increased
risk for TRH is female sex. While rigorous studies have shown that low levels of the steroid hormone estradiol
(E2) are associated with increased risk for TRH and hyper-sensitivity to threat in trauma-exposed women,
these prior studies compared women who naturally differed from one another in E2 levels regardless of
reproductive status/stage. Thus, further work is needed to determine how changes in E2 over the menopausal
transition increase vulnerability to TRH and hyper-reactivity to threat in trauma-exposed women. The current
study is well positioned to address this gap in knowledge given our recruitment of perimenopausal Black
women from a high trauma risk population. The proposed research will combine clinical interviews, fear
psychophysiology, neuroimaging, and neuroendocrinology to examine how the perimenopause and changes in
E2 levels over time influence TRH and responsivity to threat. Investigating how neuroendocrine changes
during the menopausal transition influence fear psychophysiology and amygdala reactivity to threat to impact
TRH is critical for the identification, assessment, and treatment of these symptoms during the perimenopause
in women, especially Black women, who experience disproportionately higher rates of cumulative trauma
exposure and PTSD.
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Neuroendocrine Mechanisms Underlying Perimenopausal Risk for Trauma-Related Hyperarousal in Black Women
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海外基金