A longitudinal study of cognition change during early menopausal transition in a rural community

Tzu Chi University, Hua-lien, Taiwan, Taiwan
Maturitas (Impact Factor: 2.94). 04/2006; 53(4):447-53. DOI: 10.1016/j.maturitas.2005.07.009
Source: PubMed

ABSTRACT To characterize changes in cognition that occur during the hormonal transitions of menopause.
We conducted a longitudinal population-based study in Kinmen, Taiwan, recruiting all women age 40-54 years who were premenopausal and without a history of hormone replacement therapy (HRT) or hysterectomy. The cognitive measures used to assess function included the Auditory-Verbal Learning Test, visual memory, verbal fluency, Trail Making Test and digit span.
A total of 694 eligible women participated in the baseline study, and 573 women (83%) completed follow-up 18 months later. After excluding 78 women who received hysterectomy or HRT, the final sample was composed of 495 subjects, of whom 114 (23%) progressed to perimenopause during follow-up. Women who remained premenopausal were younger than those who became perimenopausal (44.7 +/- 2.3 years versus 47.1 +/- 3.0 years, p < 0.01). All follow-up cognitive scores in women who entered perimenopause were slightly better than baseline measures except for Rey Auditory-Verbal Learning Test, which decreased by 0.23 (S.D. = 2.9, p = 0.3). At follow-up, cognitive function except for verbal fluency did not differ significantly between women who stayed premenopausal and those became perimenopausal after controlling for age, education, and baseline cognitive scores. Women who entered perimenopause have an average of 1.3 items (S.D. = 0.4) less in verbal fluency measures as compared with their premenopausal peers at the follow-up period.
The menopausal transition might not accompany significant cognitive decline except for verbal fluency.

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Available from: Jong-Ling Fuh, Sep 26, 2015
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    • "Several lines of clinical evidence suggest a rationale for the use of hormone therapy to prevent or reduce age-related cognitive decline in women. First, the loss of circulating ovarian sex steroid hormones (estrogens and progestogens) at menopause has been associated with impaired memory and executive functioning (Amore et al., 2007; Elsabagh, Hartley, & File, 2007; Fuh, Wang, Lee, Lu, & Juang, 2006; Gold et al., 2000; Halbreich et al., 1995; Thilers, Macdonald, Nilsson, & Herlitz, 2010), as well as an increased risk of Alzheimer's disease (Launer et al., 1999; Sherwin, 1999; Wolf & Kirschbaum, 2002; Yaffe et al., 2000; Yaffe, Sawaya, Lieberburg, & Grady, 1998; Zandi et al., 2002). Second, the use of estrogens in observational studies of menopausal women is associated with better verbal memory, working memory, and visuospatial function (Duff & Hampson, 2000; Duka, Tasker, & McGowan, 2000; Grodstein, Chen, Pollen, & Albert, 2000; Hogervorst, Boshuisen, Riedel, Willekes, & Jolles, 1999; Kampen & Sherwin, 1994; Maki, Zonderman, & Resnick, 2001; Matthews, Cauley, Yaffe, & Zmuda, 1999; Steffens , Norton, Plassman, & Tschanz, 1999), and with a lower risk of dementia, particularly among women who initiated treatment during, or soon after, the menopause (LeBlanc, Janowsky, Chan, & Nelson, 2001; Sherwin & Henry, 2008; Yaffe et al., 1998). "
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    ABSTRACT: A wealth of data collected in recent decades has demonstrated that ovarian sex-steroid hormones, particularly 17β-estradiol (E2), are important trophic factors that regulate the function of cognitive regions of the brain such as the hippocampus. The loss of hormone cycling at menopause is associated with cognitive decline and dementia in women, and the onset of memory decline in animal models. However, hormone therapy is not currently recommended to prevent or treat cognitive decline, in part because of its detrimental side effects. In this article, it is proposed that investigations of the rapid effects of E2 on hippocampal function be used to further the design of new drugs that mimic the beneficial effects of E2 on memory without the side effects of current therapies. A conceptual model is presented for elucidating the molecular and biochemical mechanisms through which sex-steroid hormones modulate memory, and a specific hypothesis is proposed to account for the rapid memory-enhancing effects of E2. Empirical support for this hypothesis is discussed as a means of stimulating the consideration of new directions for the development of hormone-based therapies to preserve memory function in menopausal women.
    Behavioral Neuroscience 02/2012; 126(1):29-53. DOI:10.1037/a0026660 · 2.73 Impact Factor
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    • "(huit semaines) [24] ; • mélange des stades précoces de la ménopause (caractérisées par des sécrétions anarchiques d'estrogènes) et tardifs ; • présence éventuelle de phyto-estrogènes dans l'alimentation pour celle de Fuh et al. [25] puisque cette étude a été menée chez des asiatiques dont le régime alimentaire est connu pour être riche en soja. "
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    ABSTRACT: Estrogens are neurotrophic and neuroprotective compounds. They originate from peripheral and cerebral sources. Hippocampus expresses nuclear and membrane estrogen receptors mediating dendritic spine development, synaptic plasticity and preventing elevation of intracellular Ca++ concentrations. This review examines clinical, animal and in vitro data consistently showing a preventive effect of estrogens on hippocampus-dependent memory decline with ageing. It gives a definition of phytoestrogens and presents the main data obtained in that area with these compounds. The data are consistent with those obtained with estradiol with positive and negative effects, even though the literature is scarcer. Phytoestrogens not always exhibit all estradiol-modulating effects on estrogen receptors. Several specific molecules can therefore be considered as Selected Estrogen Receptor Modulators (SERMs) and appear to be good neuro-SERMs candidates for the dietary prevention of hippocampus-dependant memory decline with ageing.
    Medecine et Longevite 03/2010; 2(1):12-21. DOI:10.1016/j.mlong.2009.09.002
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    • "However, forgetfulness is a common symptom at other ages as well, and self-reported poor memory is often more strongly linked to low mood than to objective loss of memory per­ formance (Weber and Mapstone, 2009). Crosssectional and longitudinal findings from midlife cohorts in Australia, the United Kingdom, Taiwan, Sweden and the United States are con­ sistent in suggesting that the natural menopausal transition probably has no important effect on episodic memory or on other cognitive skills (Fuh et al., 2006; Henderson et al., 2003; Herlitz et al., 2007; Kok et al., 2006; Luetters et al., 2007). Analyses from the multi-ethnic Study of Women's Health Across the Nation (SWAN) sample suggests a mild learning deficit during the menopausal transition compared to pre­ menopause, inferred from annual trends in prac­ tice effects (Greendale et al., 2009). "
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    ABSTRACT: Metabolic derangements and oxidative stress are early events in Alzheimer's disease pathogenesis. Multi-faceted effects of estrogens include improved cerebral metabolic profile and reduced oxidative stress through actions on mitochondria, suggesting that a woman's endogenous and exogenous estrogen exposures during midlife and in the late post-menopause might favourably influence Alzheimer risk and symptoms. This prediction finds partial support in the clinical literature. As expected, early menopause induced by oophorectomy may increase cognitive vulnerability; however, there is no clear link between age at menopause and Alzheimer risk in other settings, or between natural menopause and memory loss. Further, among older post-menopausal women, initiating estrogen-containing hormone therapy increases dementia risk and probably does not improve Alzheimer's disease symptoms. As suggested by the 'critical window' or 'healthy cell' hypothesis, better outcomes might be expected from earlier estrogen exposures. Some observational results imply that effects of hormone therapy on Alzheimer risk are indeed modified by age at initiation, temporal proximity to menopause, or a woman's health. However, potential methodological biases warrant caution in interpreting observational findings. Anticipated results from large, ongoing clinical trials [Early Versus Late Intervention Trial with Estradiol (ELITE), Kronos Early Estrogen Prevention Study (KEEPS)] will help settle whether midlife estrogen therapy improves midlife cognitive skills but not whether midlife estrogen exposures modify late-life Alzheimer risk. Estrogen effects on mitochondria adumbrate the potential relevance of estrogens to Alzheimer's disease. However, laboratory models are inexact embodiments of Alzheimer pathogenesis and progression, making it difficult to surmise net effects of estrogen exposures. Research needs include better predictors of adverse cognitive outcomes, biomarkers for risks associated with hormone therapy, and tools for monitoring brain function and disease progression.
    Progress in brain research 01/2010; 182:77-96. DOI:10.1016/S0079-6123(10)82003-5 · 2.83 Impact Factor
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