Contraception During Perimenopause: Practical Guidance

Grandi, Giovanni; Vinci, Pierluigi Di; Sgandurra, Alice; Feliciello, Lia; Monari, Francesca; Facchinetti, Fabio

doi:10.2147/ijwh.s288070

Cited by 5 publications

(2 citation statements)

References 93 publications

(136 reference statements)

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“…Estrogen- and progesterone-containing OCP inhibit the release of gonadotropin-releasing hormone (GnRH), suppressing levels of FSH and LH, therefore preventing follicular development and ovulation ( D’Arpe et al, 2016 ). OCP can be used to alleviate symptoms of menopause ( Grandi et al, 2022 ), representing another therapeutic option for controlling gonadotropin effects on AD risk. Generally, MRI studies show greater GMV in OCP users compared to never-users, although results are not always consistent ( Jett et al, 2022a ).…”

Section: Discussionmentioning

confidence: 99%

Elevated gonadotropin levels are associated with increased biomarker risk of Alzheimer's disease in midlife women

Nerattini,

Rubino,

Jett

et al. 2023

Front. Dement.

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IntroductionIn preclinical studies, menopausal elevations in pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), trigger Alzheimer's disease (AD) pathology and synaptic loss in female animals. Herein, we took a translational approach to test whether gonadotropin elevations are linked to AD pathophysiology in women.MethodsWe examined 191 women ages 40–65 years, carrying risk factors for late-onset AD, including 45 premenopausal, 67 perimenopausal, and 79 postmenopausal participants with clinical, laboratory, cognitive exams, and volumetric MRI scans. Half of the cohort completed 11C-Pittsburgh Compound B (PiB) amyloid-β (Aβ) PET scans. Associations between serum FSH, LH and biomarkers were examined using voxel-based analysis, overall and stratified by menopause status. Associations with region-of-interest (ROI) hippocampal volume, plasma estradiol levels, APOE-4 status, and cognition were assessed in sensitivity analyses.ResultsFSH levels were positively associated with Aβ load in frontal cortex (multivariable adjusted P ≤ 0.05, corrected for family wise type error, FWE), an effect that was driven by the postmenopausal group (multivariable adjusted PFWE ≤ 0.044). LH levels were also associated with Aβ load in frontal cortex, which did not survive multivariable adjustment. FSH and LH were negatively associated with gray matter volume (GMV) in frontal cortex, overall and in each menopausal group (multivariable adjusted PFWE ≤ 0.040), and FSH was marginally associated with ROI hippocampal volume (multivariable adjusted P = 0.058). Associations were independent of age, clinical confounders, menopause type, hormone therapy status, history of depression, APOE-4 status, and regional effects of estradiol. There were no significant associations with cognitive scores.DiscussionIncreasing serum gonadotropin levels, especially FSH, are associated with higher Aβ load and lower GMV in some AD-vulnerable regions of midlife women at risk for AD. These findings are consistent with preclinical work and provide exploratory hormonal targets for precision medicine strategies for AD risk reduction.

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Section: Discussionmentioning

confidence: 99%

Elevated gonadotropin levels are associated with increased biomarker risk of Alzheimer's disease in midlife women

Nerattini,

Rubino,

Jett

et al. 2023

Front. Dement.

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“…OCP can be used to alleviate symptoms of menopause at the perimenopausal stage 45 , representing another therapeutic option for controlling gonadotropin effects on AD risk. Generally, MRI studies show greater GMV in OCP users compared to never-users, although results are not always consistent 15 .…”

Section: Discussionmentioning

confidence: 99%

Elevated gonadotropin levels are associated with increased biomarker risk of Alzheimer’s disease in midlife women

Nerattini

Rubino

Jett

et al. 2022

Preprint

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Menopause has been implicated in women’s greater life-time risk for Alzheimer’s disease (AD) due to its disruptive action on multiple neurobiological mechanisms resulting in amyloid-β deposition and synaptic dysfunction.While these effects are typically attributed to declines in estradiol, mechanistic analyses implicate pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), in AD pathology. In transgenic mouse models of AD, increasing FSH and LH accelerate amyloid-β deposition, while inhibiting these hormones prevents emergence of AD lesions and neurodegeneration. Herein, we take a translational approach to show that, among midlife women at risk for AD, FSH elevations over the menopause transition are associated with higher amyloid-β burden, and both FSH and LH increases are associated with lower gray matter volume in AD-vulnerable brain regions. Results were independent of age, hormone therapy usage, and plasma estradiol levels. These findings provide novel therapeutic targets for sex-based precision medicine strategies for AD prevention.

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