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The temporolimbic structures of the brain that subserve emotional representation are highly epileptogenic and play an important role in the modulation of hormonal secretion and mediation of hormonal feedback. Estrogen is highly epileptogenic and exerts energizing and antidepressant effects. Excessive estrogen influence produces anxiety, agitation, irritability, and lability. It can promote the development of anxiety manifestations (e.g., panic, phobias, and obsessive-compulsive disorder). Progesterone and its metabolites inhibit kindling and seizure activity. They have potent anxiolytic effects, possibly by virtue of their GABAergic activity. Excessive progesterone influence produces sedation and depression. Testosterone has two major metabolites: estradiol, which can exacerbate seizures, and dihydrotestosterone, which blocks NMDA-type glutamate transmission and may be responsible for antiseizure effects. Testosterone has energizing effects and increases sexual desire in both men and women. In excess, however, it may promote aggressive, impulsive, and hypersexual behavior. Hormonal effects tend to be exaggerated or idiosyncratic in the setting of an abnormal or anomalous temporolimbic substrate, especially temporolimbic epilepsy. This may reflect altered neuronal responsivity to hormonal exposure perhaps by virtue of changes in the number of dendritic spines and receptors.
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PMID:Psychoneuroendocrine aspects of temporolimbic epilepsy. Part I. Brain, reproductive steroids, and emotions. 1010 Apr 30

The increasing proportion of the aged in the population is posing significant new challenges to politics, society and medicine as well. Gerontology and geriatrics are playing a role in all areas of preventive and curative medicine. Since the life expectancy of women is approximately eight years longer than that of men, gynecology draws special significance from the fact that the greater part of an aging society will primarily be comprise of women. The medical treatment and care of women in climacteric and postmenopause in the past is seriously inadequate by today's standards. The attitude in earlier years of not making any great investment of cost or personnel in patients over 75 can, in view of the vitality of modern-day senior citizens, no longer be justified or maintained. The necessity of establishing old-age gynecology becomes more and more clear and urgent. The decrease of ovarian function in menopause is without doubt an important turning point in the life of a woman. The first signs of aging are inescapable. Following these years a woman still has more than one third of life expectancy ahead of her which she would like to and should spend in good mental, spiritual and physical health. The principle of postmenopausal hormone replacement has shown itself to be amazingly successful in treating climacteric disorders and their effects on the entire organism. Treatment over many years with as board a spectrum as possible of preventive hormones to combat the long-term consequences of hormone deficiency, like osteoporosis-related fractures, heart attacks, or strokes, is one of the great medical advances of our time. Furthermore, the significance of preventing a number of genital concern manifestations through hormone replacement therapy cannot be overestimated. Gynecology has taken a remarkable step toward its goal of enabling aging women to spend the third part of their lives free of unnecessary diseases and suffering. In 1994, after consultation with representatives of European countries during the World Congress of the International Menopause Society, a statement was published by the menopause society of German-speaking countries. In this consensus paper, a stand was taken on hormone replacement therapy in postmenopause. The purpose of this paper was to serve as an aid in formulating and interpreting the text in the package inserts that are enclosed with hormone preparations. The most important passages were to once again summarize the present status of knowledge on hormone replacement therapy and its risks and benefits: (Estradiol is the estrogen normally produced by a woman's ovaries that exercises all functions of the natural follicle hormone. It is used to treat all symptoms of estrogen deficiency). Estrogen eliminates, or mitigates, all typical symptoms of estrogen deficiency in menopause, including hot flashes, night sweats and other complaints frequently observed like nervousness, sleep disturbance and depression, with great reliability. Estrogen stimulates the cell division of an aging organism, of mucous membranes, of supportive and connective tissue. It improves the blood circulation and the salt and water content. Furthermore, estrogen prevents or eliminates deterioration in the urogenital area and the disorders that result from such deterioration. Estrogen prevents or retards bone deterioration, osteoporosis and spinal, lower arm and femur fractures. By positively influencing HDL- and LDL-cholesterol, blood vessels and circulation, long-term estrogen replacement inhibits the development of arteriosclerosis and nearly halves the frequency of heart attacks and strokes. The mortality rate of women over 50 is therefore decreased significantly and life expectancy increased. (Benefits to the blood vessels of such preventive treatment can already be seen after five years of estrogen therapy and their benefits continue for several years after treatment is stopped.
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PMID:Prognostic features of menopausal and postmenopausal applicants for life insurance. 1017 66

The central nervous system is an important target for sex steroid hormones. During the climateric period the rapid decline of gonadal steroids causes neuroendocrine changes in different areas of the brain. The failure of gonadal hormone production brings specific symptoms due to the central nervous system derangement. At the hypotalamic level estrogen withdrawal gives rise to vasomotor symptoms, eating behavior disorders and altered blood pressure control. Psychological disturbances such as depression, anxiety, irritability and mood fluctuation are related to estrogen-induced changes in the lymbic system. The hypothesis of specific neuroanatomical and neurophysiological effects of estrogen on the brain may also explain the correlation between estrogen deficiency and cognitive disturbances such as Alzheimer's type dementia (AD). The increasing interest in the influence of sex steroids on brain function has focused attention on hormonal replacement therapy. Clinical and epidemiological studies have demonstrated that estrogen therapy exerts a positive effect on vasomotor instability and improves psychological disturbances. The positive effects of estrogen on mood are probably related to its stimulatory action on adrenergic and serotoninergic tone. Estrogen may influence the cognitive function through different biological actions. Estrogen administration increases total cerebral and cerebellar blood flow, cerebral glucose administration and improves cholinergic tone, a key neurotransmitter in learning and memory. The evidence suggests that hormone replacement therapy may reduce the relative risk of developing AD. Progestagens and androgen may also have a role in the control of mood disorders. At present, few data are available regarding the influence that selective estrogen receptor modulators, a new class of compounds, can exert on the brain.
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PMID:Menopause and the central nervous system: intervention options. 1022 2

Estrogen promotes neurons growth, prevents neuronal cell atrophy and regulates synaptic plasticity. Administration of estrogen protects neurons against oxidative stress, excitotoxins, and beta-amyloid-induced toxicity in cell culture. It has been shown that estrogen treatment reduces the serum monoamino oxidase levels and might regulate learning and memory. Nitric oxide (NO) is a retrograde messenger and long-term potentiation can be block using NO-synthase inhibitors or can be prevent with NO-scavengers. NO synthase is widespread in the central nervous system and acts as neurotransmitter/neuromodulator. The actions of serotonin, bradykinin, endothelin, acetylcholine and noradrenaline might be linked to NO formation. Estrogen induces activity of constitutive NO synthase and estrogen replacement therapy in postmenopausal women increases significantly circulating nitrite plus nitrate levels. The effect of estrogen on NO synthesis is rapid and is maintained with repeated administration. We demonstrated the effects of estrogen replacement therapy in Andean postmenopausal women were associated with a significantly increase in plasma levels of nitrite plus nitrate. Our hypothesis is that beneficial effect of estrogen replacement therapy on involutive depression in postmenopausal women is mediated by increase in NO production by central nervous system.
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PMID:Improvement in functions of the central nervous system by estrogen replacement therapy might be related with an increased nitric oxide production. 1047 89

Premenstrual syndrome afflicts millions of premenopausal women and has been described as one of the most common disorders in women. Research over the past few years suggests that a variety of nutrients may have an important role in the phase related mood and behavioral disturbances of the premenstrual syndrome. There is scientific evidence, at least for a few of these micronutrients, specifically calcium and vitamin D, supporting cyclic fluctuations during the menstrual cycle that may help explain some features of PMS. Ovarian hormones influence calcium, magnesium and vitamin D metabolism. Estrogen regulates calcium metabolism, intestinal calcium absorption and parathyroid gene expression and secretion, triggering fluctuations across the menstrual cycle. Alterations in calcium homeostasis (hypocalcemia and hypercalcemia) have long been associated with many affective disturbances. PMS shares many features of depression, anxiety and the dysphoric states. The similarity between the symptoms of PMS and hypocalcemia is remarkable. Clinical trials in women with PMS have found that calcium supplementation effectively alleviates the majority of mood and somatic symptoms. Evidence to date indicates that women with luteal phase symptomatology have an underlying calcium dysregulation with a secondary hyperparathyroidism and vitamin D deficiency. This strongly suggests that PMS represents the clinical manifestation of a calcium deficiency state that is unmasked following the rise of ovarian steroid hormone concentrations during the menstrual cycle.
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PMID:Micronutrients and the premenstrual syndrome: the case for calcium. 1076 3

The purpose of this review is threefold. The first objective is to assess from current literature the extent to which depressive symptoms may be associated with peri- and postmenopausal states. Although there have been many studies published addressing this topic, there remains much controversy as to whether there is a true positive correlation of increased depressive symptomatology with the peri- and postmenopausal periods. Second, sex steroid neurobiology will be reviewed. In recent years, improved technology has allowed for much more detail in investigations of the central mechanisms of action of the sex hormones. Ultimately, estrogen appears to play an excitatory role in the central nervous system, whereas progesterone has been shown to be inhibitory. The third objective is to determine whether sex steroids have been shown to clinically affect mood and psychologic function, and if so, how such information might relate to regimens for peri- and postmenopausal hormone replacement. Currently, only large, pharmacologic doses of estrogen have been shown to improve mood in clinically depressed patients. Estrogen has been shown to potentiate the effects of some antidepressants; therefore menopausal women with major depressive disorders may respond to lower doses of antidepressant medications when estrogen replacement is added to the treatment regimen.The psychological and physiological manifestations in depressive illnesses of the post-menopausal age period are of great complexity and not clearly understood. In view of the obscurity of the etiological factors it is important to isolate and study the effect of one such possible factor at a time.1Many symptoms and signs of various mood disturbances have been attributed to estrogen deficiency during the climacteric, yet it has been argued that there are no psychological symptoms specific to the menopause. The literature concerning psychological symptoms accompanying menopause is confusing.2Taken from studies published more than 50 years apart, these quotes describe the long-standing difficulty investigators have faced in evaluating psychologic function during the menopause. From the 1930s to the present, ongoing debate has surrounded issues of depression associated with the peri- and postmenopausal periods: whether there is an association at all and if so, what the cause might be and how might it be treated. Investigators continue to add new information to this debate, driven by the common understanding that issues relating to menopause and the postmenopausal period have become increasingly important. Not only are greater numbers of women approaching menopause, but these women are now expected to live greater than one third of their lives after menopause.3 The purpose of this review is first to assess from the literature the extent to which depressive symptoms may be associated with peri- and postmenopausal states. Second, in an attempt to explain or define causes of proposed changes in psychologic function during menopause, sex steroid neurobiology will be reviewed. The last objective is to determine from the literature whether sex steroids as used in hormone replacement therapy have been shown to clinically affect mood and psychological function and if so, how such information might relate to regimens for peri- and postmenopausal hormone replacement.
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PMID:Menopause and depression: a review of psychologic function and sex steroid neurobiology during the menopause(1). 1107 33

Clinical and laboratory studies suggest that progesterone reduces epileptic seizure activity. The mechanisms underlying this effect are not known. The present study determined the effects of progesterone on extracellular evoked responses recorded in the CA1 field of hippocampal slices, as well as epileptiform responses recorded from tetanized slices. Slices were prepared from ovariectomized rats, with or without estrogen replacement. Hippocampal slices were superfused in vitro with one of the following treatments: progesterone with or without RU486 (a progesterone receptor antagonist); allopregnanolone (a progesterone metabolite that potentiates GABA action at GABA(A) receptors); RU5020 (a high-affinity progesterone receptor agonist); or cholesterol (control). In non-tetanized slices, a twofold increase in the excitatory postsynaptic field potential and population spike amplitude occurred during both cholesterol and progesterone superfusion. In contrast, under the same conditions, exposure to allopreganolone caused a 25% reduction in both field potential and population spike amplitude of evoked responses within 30min of treatment. In tetanized slices, progesterone and RU5020, but not allopregnanolone or cholesterol, caused significant reductions in the field potential and population spike amplitude of evoked responses. Progesterone and RU5020 also significantly reduced the duration of tetanic stimulus-induced afterdischarges and the frequency of spontaneous interictal discharges. The effects of allopregnanolone were restricted to a reduction in the primary afterdischarge duration. Estrogen replacement slightly attenuated progesterone's suppression of spontaneous discharges and depression of evoked responses. All responses to progesterone were blocked by prior or concurrent exposure to RU486. These data indicate that allopregnanolone suppresses evoked potentials in non-tetanized hippocampal slices, consistent with previous reports that this neurosteroid has marked anxiolytic and anticonvulsant effects. After tetanization, however, progesterone receptor-mediated responses become quantitatively more important as a mechanism for suppressing hippocampal electrical activity.
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PMID:Progestin receptors mediate progesterone suppression of epileptiform activity in tetanized hippocampal slices in vitro. 1111 38

Estrogen exerts profound effects on mood and mental state. The ability of estrogen to modulate serotonergic function raises the possibility that it may play a role in the mechanism associated with depression and its treatment. A cellular mechanism for estrogen to influence mood might be through the regulation of genes involved at various levels of the serotonin system. Here we report that estrogen can up-regulate the expression of the serotonin-1A receptor via a new mechanism involving synergistic activation by nuclear factor-kappa B (NF-kappa B) with estrogen receptor alpha. Interestingly, we observed that only estrogen receptor-alpha, and not -beta, was able to mediate this effect of estrogens. The partial antiestrogen, 4-hydroxytamoxifen, had the same effect as estrogen. In addition, mutation analysis showed that both the transactivation function of p65 and activation function 1 of estrogen receptor-alpha were essential for this synergistic regulation. Therefore, we propose that NF-kappa B complexes cooperate with estrogen receptor-alpha to recruit cofactors into the complex and thereby synergistically activate the serotonin-1A receptor promoter through nonclassical estrogen response elements by a mechanism that does not involve direct receptor binding to DNA.
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PMID:Synergistic activation of the serotonin-1A receptor by nuclear factor-kappa B and estrogen. 1126 6

How a weakened immune system affects the female's reproductive system is explained. The female's endocrine system controls the menstrual and reproductive systems, and the immune system attacks harmful substances and organisms. The hypothalamus stimulates the pituitary gland to produce the hormones FSH and LH, which in turn signal the ovaries to produce estrogen and progesterone. These hormones cause a mature egg to be released. If fertilized, the egg remains within the uterus; if not, menstruation occurs. HIV-positive females often complain of menstrual cycle changes, such as irregular periods, depression, or pain. The virus, other complications, or medications, such as AZT, may cause these symptoms. Estrogen therapy may help those with suppressed immune systems who have premature menopause. Oral contraceptives offer protection against pregnancy, but not HIV. It is not known if the pill reacts adversely with AIDS treatment drugs. Lists are provided showing the pros and cons of oral contraceptives and hormone therapy.
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PMID:[Women, immunity and sexual hormones]. 1136 3

The benefit of treating postmenopausal women with established cardiovascular disease with combined estrogen-progestogen hormone replacement therapy (HRT) is controversial. This study investigated the effect of treatment with estradiol and norethisterone acetate on exercise tolerance and on the frequency and severity of ischemic attacks in postmenopausal women with stable angina pectoris. A total of 74 Chinese women were recruited for this 16-week double-blind, placebo-controlled trial. They were randomly allocated into two groups; one group received placebo/placebo/placebo and the other group received placebo/estrogen-progestogen/placebo. Estrogen-progestogen continuous combined HRT increased both time to 1-mm ST depression (99.1 s, p < 0.05) compared with a mean decrease of 22.9 s with placebo (p < 0.05), and total exercise duration also showed a significant increase (32.7 s, p < 0.05) after treatment compared with placebo (2.5 s, p < 0.05). In addition, the total number of ischemic events/24 h during ambulatory electrocardiographic monitoring decreased by 0.82 events after treatment (p < 0.05) compared with an increase in the placebo group (0.94), a highly significant difference (p = 0.006). These results suggest that the administration of this particular combined hormone replacement preparation may have a beneficial effect on myocardial ischemia in postmenopausal women with established coronary disease.
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PMID:Anti-ischemic action of estrogen-progestogen continuous combined hormone replacement therapy in postmenopausal women with established angina pectoris: a randomized, placebo-controlled, double-blind, parallel-group trial. 1148 42


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