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Effects of early surgical menopause on sleep, memory, and medial temporal lobe structure at midlife
Author(s) -
Gervais Nicole J,
Lauzon Claire,
Brown Alana,
Gravelsins Laura,
Nicoll Gina,
BakerSullivan Elizabeth,
Almey Anne,
Reuben Rebekah B,
Duchesne Annie,
Mendoza Leanne,
Perovic Mateja,
Kannampuzha Courtney,
Grady Cheryl,
Olsen Rosanna,
Einstein Gillian
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.047548
Subject(s) - entorhinal cortex , atrophy , medicine , dementia , temporal lobe , cognitive decline , menopause , audiology , psychology , polysomnography , sleep disorder , hippocampus , cognition , neuroscience , disease , epilepsy , apnea
Background Women bear the greatest burden of Alzheimer’s disease (AD) with menopause‐associated estrogen (E) loss becoming increasingly implicated. Surgical menopause <45 years of age (via bilateral salpingo‐oophorectomy, BSO) is thought to further increase the risk (Rocca et al., 2007). Neurodegeneration and atrophy in medial temporal lobe (MTL) structures including the perirhinal (PRC) and entorhinal (ERC) cortices occur in the very early stages of AD (e.g. Khan et al., 2013; Wolk et al., 2017). Further, sleep disturbance is also implicated in AD progression (Lim et al., 2013). Unknown is whether BSO‐associated sleep disturbance contributes to reduced memory performance and MTL atrophy via sleep disturbance, and whether E2 supplementation influences this relation. Our study aimed to determine the effect of early hormone deprivation (via BSO) on MTL volume, visual recognition memory, and whether this is correlated with sleep disturbance. Method Demographic and cognitive measures were administered to women with an oophorectomy <45 years who were either taking estradiol‐based hormone therapy (BSO+E2: n =19), or not taking E2 (BSO no E2: n =15). Data was also collected from age‐matched premenopausal women (AMC: n =27). High‐resolution T2‐weighted scans were acquired using a Siemens 3T Prisma scanner, and hippocampal subfields, PRC, ERC, and parhippocampal cortex were manually segmented (Olsen et al., 2017) in FSLView. The interference match‐to‐sample (IMTS) task was used to asses and recognition memory (Watson et al., 2013). Sleep was assessed using an at‐home polysomnography device (Vitaport‐5/REMbo‐234, Temec Technologies). Result Relative to AMCs, the BSO no E2 group had smaller volumes in the dentate gyrus, CA2, and CA3 (DGCA23) ( p <.05, d =1.03). Relative to BSO+E2 women with BSO no E2 had reduced recognition memory performance ( p <.05; d =1.36) and their sleep was more disrupted, indicated by increased sleep latency ( p <.05, d =.71), and cortical arousals ( p <.05, d =.87]. DGCA23 volume and nighttime arousals were correlated negatively ( r= ‐.503, p <.05). Conclusion Our findings demonstrate that HPC, recognition memory, and sleep are sensitive to E2 loss and suggest that reduced HPC volume relates to disrupted sleep. Taken together these findings begin to explicate the path from early menopause to late‐life dementia and the importance of E2 for women’s brain health.