Showing papers by "David R. Rubinow published in 2000"
TL;DR: The data provide direct evidence in support of the involvement of the reproductive hormones estrogen and progesterone in the development of postpartum depression in a subgroup of women and suggest that women with a history of post partum depression are differentially sensitive to mood-destabilizing effects of gonadal steroids.
Abstract: OBJECTIVE: Endocrine factors are purported to play a role in the etiology of postpartum depression, but direct evidence for this role is lacking. The authors investigated the possible role of changes in gonadal steroid levels in postpartum depression by simulating two hormonal conditions related to pregnancy and parturition in euthymic women with and without a history of postpartum depression.METHOD: The supraphysiologic gonadal steroid levels of pregnancy and withdrawal from these high levels to a hypogonadal state were simulated by inducing hypogonadism in euthymic women—eight with and eight without a history of postpartum depression—with the gonadotropin-releasing hormone agonist leuprolide acetate, adding back supraphysiologic doses of estradiol and progesterone for 8 weeks, and then withdrawing both steroids under double-blind conditions. Outcome measures were daily symptom self-ratings and standardized subjective and objective cross-sectional mood rating scales.RESULTS: Five of the eight women with ...
802 citations
TL;DR: In this preliminary study estradiol replacement effectively treats perimenopausal depression independent of its salutary effects on vasomotor symptoms.
553 citations
TL;DR: It is concluded that TNF-α may up-regulate GFAP through the MAPK signaling pathway, a hallmark of reactive gliosis, and understanding the mechanisms that regulate GFAP expression may facilitate development of strategies to minimize the gliosis associated with many brain diseases.
Abstract: Increased levels of tumor necrosis factor-alpha (TNF-alpha), a pluripotent cytokine that is reportedly mitogenic to astrocytes, are associated with the expression of glial fibrillary acidic protein (GFAP), the most specific marker for astrocytes, in many neuropathological conditions, including brain injury, CNS infection, Creutzfeldt-Jakob disease and Alzheimer's disease. Here, we show that treatment of cultured astrocytes with TNF-alpha resulted in dramatic over-expression of GFAP, associated with a substantial activation of the mitogen activated protein kinase (MAPK) Erk2 (extracellular signal-regulated protein kinase). We also demonstrate that TNF-alpha-induced over-expression of GFAP was significantly attenuated by the MAPK inhibitor PD98059. We conclude that TNF-alpha may upregulate GFAP through the MAPK signaling pathway. Because increased GFAP is a hallmark of reactive gliosis, understanding the mechanisms that regulate GFAP expression may facilitate development of strategies to minimize the gliosis associated with many brain diseases.
52 citations
TL;DR: The results suggest that E and T differ in effect on differentiation, while neither affect proliferation in early developmental cortex, and since the AR is expressed in the cortical neurons by E14, the inhibitory effect of T on differentiation may be receptor-mediated, while the stimulatory effects of estrogen in the cortex do not appear to involve nuclear ER(alpha) at this developmental stage.
41 citations
TL;DR: Three patients who demonstrated rapid improvement in symptoms of irritability, hostility, and behavioral disinhibition after treatment with low-dose risperidone are reported.
7 citations
5 citations
TL;DR: It is demonstrated that sex steroids regulate several measures of CNS function, however, the direction and patterns of effects vary with context including age and gender.
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