The other side of estrogen replacement therapy: Outcome study results of mood improvement in estrogen users and nonusers

Miller, Karen J.

doi:10.1007/s11920-003-0082-5

Cited by 21 publications

(9 citation statements)

References 59 publications

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“…Neuropsychiatrists have also conceded that 'there is a clear need to examine the necessary duration of HRT for neuroprotection to decrease a woman's risk for depression, cognitive dysfunction and development of Alzheimer's disease' 44 .…”

Section: Climacteric Depressionmentioning

confidence: 99%

Hormones and depression in women

Studd

Panay

2004

Climacteric

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The biological plausibility for the effect of sex hormones on the central nervous system is now supported by a considerable amount of clinical data. This critical review guides the reader through the plethora of data, from the earliest reports of menstrual madness in the nineteenth century to neurobiological work in the new millennium. It illustrates through the scientific evidence base that, although the effect of estrogen on the central nervous system, particularly on mood and depression, remains a controversial area, there is now considerable evidence for the psychotherapeutic benefits of estrogens in the triad of hormone-responsive depressive disorders: postnatal depression, premenstrual depression and perimenopausal depression. The article also reviews the compelling data that testosterone supplementation has positive effects for depression, libido and energy, particularly where patients have only partially responded to estrogen therapy.

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Section: Climacteric Depressionmentioning

confidence: 99%

Hormones and depression in women

Studd

Panay

2004

Climacteric

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“…A. Morgan et al, 2004), spatial learning (H. N. Fugger et al, 1998), mood and cognition (K. J. Miller, 2003; C.…”

Section: Introductionmentioning

confidence: 99%

The gad2 Promoter Is a Transcriptional Target of Estrogen Receptor (ER) and ER : A Unifying Hypothesis to Explain Diverse Effects of Estradiol

Hudgens

Lan²,

Carpenter³

et al. 2009

Journal of Neuroscience

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Estradiol (E 2 ) regulates a wide range of neural functions, many of which require activation of estrogen receptor ␣ (ER␣) and/or ER␤, ligand-gated transcriptional regulators. Surprisingly, very few neural gene targets of ERs have been identified, and these cannot easily explain the myriad effects of E 2 . GABA regulates most of the same neural functions as E 2 , and GABAergic neurons throughout the brain contain ER. Therefore, we examined whether E 2 directly regulates expression of glutamic acid decarboxylase 2 (gad2), the enzyme primarily responsible for GABA synthesis for synaptic release. Using dual luciferase assays, we found that E 2 , but not other gonadal steroids, stimulated the activity of a 2691 bp rat gad2 promoter reporter construct. Activation required either ER␣ or ER␤, and ER␤ did not repress ER␣-mediated transactivation. Site-directed mutagenesis studies identified three estrogen response elements (EREs) with cell-specific functions. An ERE at Ϫ711 upstream of the gad2 translational start site was essential for transactivation in both MCF-7 breast cancer cells and SN56.B5.G4 neural cells, but an ERE at Ϫ546 enhanced transcription only in neural cells. A third ERE at Ϫ1958 was inactive in neural cells but exerted potent transcriptional repression in E 2 -treated MCF-7 cells. Chromatin immunoprecipitation assays in mouse GABAergic N42 cells confirmed that E 2 induced ER␣ binding to a DNA fragment containing sequences corresponding to the Ϫ546 and Ϫ711 EREs of the rat promoter. Based on these data, we propose that direct transcriptional regulation of gad2 may explain, at least in part, the ability of E 2 to impact such a diverse array of neural functions.

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“…Although some studies (Zweifel and Obrien, 1997;Miller, 2003) suggest that HRT augments serotonergic activity and facilitates the improvement of clinical depression and the efficacy of antidepressants, other studies (Pearce et al, 1997) do not report an antidepressant effect from HRT. This study showed that HRT alone did not alleviate depressive symptoms in menopausal women.…”

Section: Discussionmentioning

confidence: 99%

Frontal Cerebral Blood Flow Changes after Hormone Replacement Therapy in Depressed Postmenopausal Women

Yao

Pan

Wang

et al. 2009

J Cereb Blood Flow Metab

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We investigated the effects of hormone replacement therapy (HRT) on frontal cerebral blood flow (CBF), depressive symptoms, and cognitive function in depressed postmenopausal women. Fourteen postmenopausal women with depressive symptoms underwent HRT, and seven controls not undergoing HRT were studied. We evaluated frontal CBF, expressed as frontal/cerebellum (F/C) ratio, using Tc-99m hexamethyl propylene amine oxime single photon emission computed tomography (Tc-99m HMPAO SPECT), cognitive function using the Mini-Mental Status Examination (MMSE), and depression using the HAD (Hospital Anxiety and Depression) scale. All studies were carried out at initial status and after 9 months. Single photon emission computed tomography was performed at rest and at activation during the Wisconsin Card Sorting Test (WCST). Initial frontal CBF was not different between groups. After 9 months, resting frontal CBF was similar between groups. However, activated frontal CBF was significantly higher in the HRT group than in controls (F/C ratio: 0.924±0.04 versus 0.853±0.05, P=0.007). Furthermore, the increase in the activated F/C ratio was inversely associated with years since menopause. Mini-Mental Status Examination scores improved after HRT, but depression scores did not. Hormone replacement therapy improved frontal CBF and cognitive function but not depression in postmenopausal women. The changes in frontal CBF were detected only during WCST activation and were most apparent during early postmenopausal years.

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The other side of estrogen replacement therapy: Outcome study results of mood improvement in estrogen users and nonusers

Cited by 21 publications

References 59 publications

Hormones and depression in women

Hormones and depression in women

The gad2 Promoter Is a Transcriptional Target of Estrogen Receptor (ER) and ER : A Unifying Hypothesis to Explain Diverse Effects of Estradiol

Frontal Cerebral Blood Flow Changes after Hormone Replacement Therapy in Depressed Postmenopausal Women

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