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
摘要
在社会经济水平较低的城市黑人社区,重复创伤暴露的累积比率较大
这种状况与创伤后不良心理健康后果的发生率增加有关,
包括创伤后应激障碍(PTSD)。创伤后应激障碍与创伤相关过度觉醒(TRH)相关
以及依赖于调节对威胁反应的大脑区域的失调的恐惧反应,
包括杏仁核和前额叶腹内侧皮质。一种生物因素导致增加
患TRH的风险是女性。虽然严格的研究表明,低水平的类固醇激素雌二醇
(E2)与创伤暴露妇女中TRH风险增加和对威胁高度敏感有关,
这些先前的研究比较了雌激素水平自然不同的女性,而不考虑
生殖状态/阶段。因此,需要进一步的工作来确定绝经后雌二醇的变化。
在创伤暴露的妇女中,过渡增加了TRH的易感性和对威胁的高反应性。海流
鉴于我们招募的围绝经期黑人,这项研究处于很好的地位来解决这一知识差距
来自创伤高危人群的女性。这项拟议的研究将结合临床访谈、恐惧
心理生理学,神经成像和神经内分泌学,以检查围绝经期和
随着时间的推移,E2水平会影响TRH和对威胁的响应性。研究神经内分泌如何变化
更年期过渡期对恐惧感、心理生理学和杏仁核反应性的影响
TRH对围绝经期这些症状的识别、评估和治疗至关重要。
在女性中,特别是黑人女性,她们经历了不成比例的累积创伤
暴露和创伤后应激障碍。
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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会议论文
Neuroendocrine Mechanisms Underlying Perimenopausal Risk for Trauma-Related Hyperarousal in Black Women
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海外基金