雌激素与女性认知功能关系的研究进展

随着女性平均预期寿命的延长及阿尔茨海默病(alzheimer disease,AD)的发病率明显上升,雌激素与女性认知功能的关系研究成为当今学术界研究的热点之一。细胞培养和动物实验数据已经证实,雌激素能通过多种途径保护认知功能相关区域的神经细胞,进而提高认知功能。但是学者们对雌激素水平和女性认知功能的相关性问题,及激素补充治疗(HRT)对围绝经期及绝经后女性认知功能是否有保护作用仍有争议。多数研究表明雌激素水平和女性认知功能是相关的,但是不同的人群,不同时期,不同的认知测试可能会有不同结果。激素补充治疗能否提高女性认知功能取决于研究人群、治疗时机、药物种类及个体化用药等。     

雌激素对绝经后妇女脑功能影响的研究进展

雌激素有保护脑血管和神经的作用。绝经后低雌激素血症是影响妇女脑血管和神经营养的高危因素。外源性雌激素能明显改善脑功能 ,对防治绝经后妇女脑血管疾病和早老性痴呆有一定的意义     

绝经后激素治疗与认知及记忆功能

雌激素改善脑认知功能的作用早在20世纪70年代开始被人们认识,实验室和动物研究发现雌激素有神经保护功能且其机制复杂,许多研究显示绝经后激素治疗可降低与老年性痴呆有关的痴呆危险性并改善部分认知功能。近期研究发现激素治疗可通过增加脑萎缩这一机制增加大于65岁以上老年绝经后妇女认知障碍,激素治疗不能用于老年绝经后妇女认知功能的一级预防。     

长链非编码RNA在绝经后认知功能减退中的研究进展

长链非编码RNA参与多种疾病的发生发展过程,与神经系统退行性疾病尤其是认知功能障碍密切相关.较多证据表明女性绝经后存在认知功能减退.目前尚无关于lncRNA在绝经后认知功能减退中的直接研究,但间接证据表明雌激素与影响神经功能的lncRNA关系密切.文章就lncRNA在绝经后认知功能减退的发生发展中的作用展开综述.     

雌激素替代疗法在防止骨质疏松中的作用

因卵巢衰竭而引起的月经闭止——绝经,可考虑为一种内分泌病理。雌激素水平的明显下降可有许多不良的后果,包括潮红、泌尿生殖道萎缩,心血管疾病的增加和骨质疏松。骨质疏松的定义是单位体积骨质减少而矿物质/基质比为正常。骨质疏松患者骨矿物质密度为同种属同性别的正常青年期的80%以下。妇女中最常见的骨质疏松原因为绝经后低雌激素,也可在绝经年龄前后及低雌激素性闭经中发生。它的许多高危因素有:女性,白人或亚洲系人群,有家族史     

雌激素对女性心血管系统保护作用的研究

雌激素是一种类固醇激素,可作用于心血管系统、生殖系统等众多靶器官。研究表明,雌激素除了调控生殖系统以外,在预防心血管疾病等方面有十分重要的临床价值。心血管系统疾病是女性死亡的主要原因,绝经后妇女冠心病的发病率增加与绝经后体内雌激素水平的大幅度减少密切相关。几十年来,激素替代疗法尤其是雌激素替代疗法一直作为绝经后妇女疾病预防的主流疗法,但其是否具有心脏保护效应一直存在争议。本文就近年来雌激素对心血管活动影响机制的研究结果以及激素替代疗法对心血管系统疾患的疗效分析进行总结。     

雌激素与女性骨关节炎

骨关节炎(OA)是老年人常见慢性疾患,其患病率存在显著性别差异.绝经后妇女OA患病率增加,明显高于同龄男性,而绝经后雌激素水平显著低于正常,提示雌激素在OA发病中起重要作用.有关雌激素对OA的影响研究结果不一致,多数体内和体外动物试验研究结果提示雌激素对OA有保护作用,可抑制软骨下骨转换和软骨蛋白多糖降解,保持软骨厚度,减轻OA病变.现有流行病学研究显示绝经后雌激素治疗可降低OA患病率,减轻OA症状,而另一些结果则相反.对现有流行病学和实验室研究证据进行综述,探讨雌激素与女性骨关节炎之间的关系.     

雌激素与女性骨关节炎

骨关节炎（OA）是老年人常见慢性疾患，其患病率存在显著性别差异。绝经后妇女OA患病率增加，明显高于同龄男性，而绝经后雌激素水平显著低于正常，提示雌激素在OA发病中起重要作用。有关雌激素对OA的影响研究结果不一致，多数体内和体外动物试验研究结果提示雌激素对OA有保护作用，可抑制软骨下骨转换和软骨蛋白多糖降解，保持软骨厚度，减轻OA病变。现有流行病学研究显示绝经后雌激素治疗可降低OA患病率，减轻OA症状，而另一些结果则相反。对现有流行病学和实验室研究证据进行综述。探讨雌激素与女性骨关节炎之间的关系。     

雌激素对听力损失影响的研究进展

雌激素是一种具有多种功能的类固醇类激素。近年来的研究发现,外周血雌激素水平的变化会对听力产生影响,例如,女性在绝经会出现高频听力损失;绝经后给予外源性雌激素补充后,听力损失恢复等。目前研究证明,雌激素对听力损失影响的机制主要有以下几个方面:①雌激素受体在听觉传导通路上表达的分布决定了雌激素对听力的作用,同时,雌激素受体基因异常表达和多态性也会影响雌激素对听力的作用;②雌激素可通过对听觉上皮细胞修复而保护听力;③雌激素浓度可通过改变耳蜗血管纹的代谢和血流速度,进而影响听力水平;④雌激素可通过促进脑源性神经营养因子相关基因表达、抑制细胞凋亡和调节钙离子浓度平衡,进而保护听神经细胞。对雌激素与听力之间的关系及其影响机制的综述和探讨,能够为临床雌激素相关的听力减退的治疗提供理论依据和解决方案。     

雌激素和上皮性卵巢肿瘤的关系研究进展

卵巢癌发生的分子机制尚不清楚.临床和实验室证据表明,雌激素可促进上皮性卵巢肿瘤(EOC)的发展.实验证明,雌激素可促进表达雌激素受体(ER)的卵巢肿瘤细胞的生长.卵巢癌发生过程中有ERα或β亚型表达的改变.雌激素诱导生成的蛋白如c-myc、细胞外基质蛋白fibulin-1可能在EOC发生中起作用.前瞻性流行病学研究表明,绝经后妇女的雌激素替代疗法可增加卵巢癌的发生率和死亡率.因而,应重新评价EOC对雌激素治疗的敏感性.     

Homocysteine, estrogen and cognitive decline.

BACKGROUND: Factors that contribute to cognitive decline in women from midlife remain poorly understood. There are circumstantial data indicating a positive association between homocysteine and cognitive decline and that endogenous and exogenous estrogen may influence homocysteine levels. The aim of this review was to establish what is known of the relationships between cognitive change and homocysteine levels, and the impact of the menopause transition and exogenous estrogen on homocysteine levels. METHODS: We reviewed the recent published literature from 1993 to 2005 pertaining to the current understanding of the relationship(s) between plasma homocysteine levels and cognitive functioning and endogenous hormone levels and exogenous estrogen use in women. RESULTS: Hyperhomocysteinemia is consistently associated with cognitive decline. Dietary supplementation with vitamins may assist in normalizing homocysteine levels; however, there is no evidence that this results in favorable effects on cognition. Changes in endogenous estrogen levels are inversely associated with changes in serum homocysteine. Consistent with this, estrogen therapy is associated with reductions in plasma homocysteine, with the greatest effects reported in women with higher levels of homocysteine at baseline. Limited data indicate that tibolone is associated with little change in homocysteine. The use of raloxifene, the most studied selective estrogen receptor modulator, is associated with a modest reduction in homocysteine. CONCLUSIONS: There are data to suggest an underlying link between homocysteine levels and cognitive decline. There is also evidence for a link between both the menopause transition and use of exogenous estrogen therapy and homocysteine levels. Clinical data do not support a role for exogenous estrogen in the prevention of dementia in older women; however, the 'window of opportunity' theory suggests that there is a need for randomized controlled trials to evaluate the role of estrogen in the early postmenopausal years to protect against cognitive decline in later life.     

Effect of estrogen and testosterone replacement therapy on cognitive fatigue

Both estrogen and testosterone insufficiency has been associated with reduced psychological well-being including fatigue. However, hormonal replacement studies on fatigue are rare. Therefore, we wanted to study the effect of testosterone and estrogen replacement therapy on cognitive fatigue and the relation between sex hormone levels and cognitive fatigue in oophorectomized women. Fifty women with surgically induced menopause (mean age: 54.0?±?2.9 years) were randomly assigned to treatment with estradiol valerate in combination with testosterone undecanoate or placebo for 24 weeks in a double-blind cross-over study. Neuropsychological tests and questionnaires were used to assess cognitive fatigue and psychological well-being. Cognitive fatigue was significantly associated to poor self-rated health and higher body mass index but not to general psychological well-being or sex hormone levels. Treatment with testosterone + estrogen had no significant effect on cognitive fatigue but the results indicated a curvilinear relation for hormonal levels. The estrogen/testosterone ratio was more related to functions rather than high or low hormone levels per se. We found that cognitive fatigue is frequent in oophorectomized women and negatively associated to self-perceived health and positively associated to BMI. A well-balanced ratio between estrogen and testosterone levels may be important for cognitive fatigue.     

早发性卵巢功能不全对神经功能影响

多数观察性研究表明,低雌激素状态对精神神经功能和认知功能有影响,在早发性卵巢功能不全(POI)患者表现更为明显,但直接的研究证据或高级别循证医学研究的评估资料有限。对POI患者尽早开始激素补充治疗有利于预防或减缓神经功能的退化或下降,但并不能完全纠正过早的卵巢功能衰退和绝经对神经功能的负面影响。重视POI发生和进展的各项影响因素,尽可能减缓病程进展,是防范POI患者神经功能损伤的首要措施。     

Cardiovascular disease as a current threat of older women. Relation to estrogens

Cardiovascular disease (CVD) is the leading cause of death in women around the world. Cardiovascular disease risk increases after the menopause which may be related to metabolic and hormonal changes. The decline in ovarian function with menopause is associated with spontaneous increases in proinflammatory cytokines. Chronic inflammation is a major factor that drives the progression of atherosclerosis and atherothrombosis. Measurement of the inflammatory markers has been postulated as a method of determining increased risk of cardiovascular disease in apparently healthy older women. Endogenous estrogen appears to be cardioprotective and several observational epidemiological studies have suggested that hormone therapy reduces the risk of coronary events in healthy postmenopausal women. However, recent clinical studies failed to show such beneficial effect. Among the mechanism that may account for the effects of hormone therapy on cardiovascular disease is inflammation.     

Cognitive changes after menopause: influence of estrogen

The natural menopause is not associated with substantial cognitive change. Limited clinical trial evidence suggests that estrogen-containing hormone therapy has little effect on cognition during midlife, but prompt initiation after surgical menopause may improve aspects of memory. Among older postmenopausal women, strong clinical trial evidence demonstrates that hormone initiation does not improve cognition. More limited clinical trial evidence indicates no improvement in Alzheimer symptoms, and the Women's Health Initiative Memory Study found an increase in dementia risk among older women. Observational findings of reduced Alzheimer risk may reflect early hormone use in younger women, or findings may be biased. Cognitive effects of selective estrogen receptor modulators are not yet well studied.     

Menopause and disorders of the central nervous system

The cessation of ovarian estrogen production occurring around the time of menopause has the potential to influence central nervous system function, as well as a number of neurological disorders that affect women during midlife and old age, including memory loss and mild cognitive impairment, ischemic stroke, Parkinson's disease, and Alzheimer's disease. During midlife, there is observational evidence that episodic memory is not substantially affected by natural menopause or by use of estrogen-containing hormone therapy, but short-term clinical trial evidence suggests hormone therapy might benefit verbal memory after surgical menopause. Clinical trial data indicate that hormone therapy does not reduce, and may increase, stroke incidence. Parkinson's disease and Alzheimer's disease are the 2 most common neurodegenerative illnesses. Estrogen influences dopaminergic pathways within the central nervous system. However, available observational evidence is limited and inconclusive regarding any role of hormone therapy in influencing risk or symptoms of Parkinson's disease, a disorder of dopaminergic neurons. Finally, clinical trial data indicate that hormone therapy should not be initiated in the late postmenopause with the goal of improving memory, preventing cognitive decline, reducing dementia risk, or improving Alzheimer's disease symptoms. An important priority for clinical investigation is to determine whether hormone therapy used during the menopausal transition and early postmenopause has long-term effects on cognition or dementia risk. The critical window hypothesis as applied to Alzheimer's disease conjectures that effects of early hormone therapy might differ from those of hormone therapy initiated in the late postmenopause, but convincing evidence is yet to be obtained.     

Alzheimer’s disease in postmenopausal women: screening for cognitive decline in the OB/GYN office

Alzheimer’s disease is the most common cause of dementia diagnosed today, affecting nearly 10% of Americans over the age of 65. The prevalence of this neurodegenerative disease has been escalating and will continue to rise as the population ages. Recent studies suggest that estrogen deficiency in postmenopausal women increases the risk for Alzheimer’s disease and that hormone replacement therapy may prevent or delay disease progression. Therefore, OB/GYN physicians are becoming more interested in the potential prevention, detection and treatment of Alzheimer’s disease in menopausal patients. In response, we recommend that OB/GYNs incorporate a cognitive self-assessment tool, such as the self-administered questionnaire we have developed, in an attempt to recognize and follow the course of cognitive function in their ambulatory patients. Recognition of early cognitive decline will be increasingly important as novel treatments to delay disease progression emerge. This paper reviews the current etiology of Alzheimer’s disease, the effects of estrogen on brain function, and presents a prototype of a Cognitive Self-Assessment tool OB/GYNs can use in their office setting for following cognitive function in patients.     

Sexualität und Testosteronsubstitution in der Menopause

The time of menopause and postmenopause is characterized by multiple changes to the female body and psyche. Although the majority of these symptoms are caused by the well-known decline of estrogen levels, studies suggest that the effects of falling testosterone levels with age or after a bilateral oophorectomy may also play a role in this setting, showing a negative impact on sexual functioning. Today, several options exist for the treatment of the symptoms associated with menopause. Estrogen deficiency-associated symptoms can be treated with systemic hormone replacement therapy and topical preparations for the genitalia. A new transdermal system for the administration of testosterone may be used in women who are already being treated with estrogens and who are suffering from HSDD that occurred after hysterectomy and bilateral oophorectomy.     

Effects of female sex hormones on caffeine-induced epileptiform activity in rats

Research on female sex hormones has demonstrated that estrogen aggravates epileptogenesis. Theoretically, this means that the frequency of epileptic attacks should be decreased in epileptic women during menopause. However, although epilepsy attacks are reported to decrease in some women during menopause, they may not change in others. Increases in attack frequency have even been reported during menopause in some epileptic women. This study has investigated the effects of estrogen, progesterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) on caffeine-induced epileptiform activity in rats. Estrogen was found to increase epileptiform activity in a dose-dependent manner via its own receptors. In contrast, progesterone had no effect on epileptiform activity. FSH and LH suppressed epileptiform activity at low doses; however, at high doses they enhanced it. In conclusion, we suggest that the occurrence or aggravation of epilepsy, despite estrogen deficiency in the menopausal or post-menopausal period, is related to excessive accumulation of FSH and LH.