Estrogen Receptor Genes, Cognitive Decline, and Alzheimer Disease
Open accessAbstract
Background and Objectives Lifetime risk of Alzheimer disease (AD) dementia is twofold higher in women compared with men, and low estrogen levels in postmenopause have been suggested as a possible contributor. We examined 3 ER (GPER1, ER2, and ER1) variants in association with AD traits as an indirect method to test the association between estrogen and AD in women. Although the study focus was on women, in a comparison, we separately examined ER molecular variants in men. Methods Participants were followed for an average of 10 years in one of the 2 longitudinal clinical pathologic studies of aging. Global cognition was assessed using a composite score derived from 19 neuropsychological tests9 scores. Postmortem pathologic assessment included examination of 3 AD (amyloid-β and tau tangles determined by immunohistochemistry, and a global AD pathology score derived from diffuse and neurotic plaques and neurofibrillary tangle count) and 8 non-AD pathology indices. ER molecular genomic variants included genotyping and examining ER DNA methylation and RNA expression in brain regions including the dorsolateral prefrontal cortex (DLPFC) that are major players in cognition and often have AD pathology. Results The mean age of women (N = 1711) at baseline was 78.0 (SD = 7.7) years. In women, GPER1 molecular variants had the most consistent associations with AD traits. GPER1 DNA methylation was associated with cognitive decline, tau tangle density, and global AD pathology score. GPER1 RNA expression in DLPFC was related to cognitive decline and tau tangle density. Other associations included associations of ER2 and ER1 sequence variants and DNA methylation with cognition. RNA expressions in DLPFC of genes involved in signaling mechanisms of activated ERs were also associated with cognitive decline and tau tangle density in women. In men (N = 651, average age at baseline: 77.4 [SD = 7.3]), there were less robust associations between ER molecular genomic variants and AD cognitive and pathologic traits. No consistent association was seen between ER molecular genomic variations and non-AD pathologies in either of the sexes. Discussion ER DNA methylation and RNA expression, and to some extent ER polymorphisms, were associated with AD cognitive and pathologic traits in women, and to a lesser extent in men.
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Transcriptome-wide sex differences in AD have been characterized in multiple studies.
“While transcriptome‐wide sex differences in AD have been characterized in multiple studies, 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 proteome‐wide sex differences in AD remain underexplored.”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [16]
The RNA Expression Processing section describes transcriptome-scale sequencing, and the Discussion reports different associations between estrogen-receptor molecular variants and AD traits in women and men. But the analyses focus on selected estrogen-receptor genes and their pathways; this paper does not characterize transcriptome-wide sex differences in AD. (LLM, conf=0.85)
Experimental — accuracy not yet measuredEstrogen receptor expression has stronger associations with AD cognitive and pathologic traits in females than males.
“Expression of the estrogen receptor had stronger associations with AD cognitive and pathologic traits in females than males.”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [16]
Our results corroborate previous studies that highlighted a sex-specific association between AD and estrogen receptors.
“Our results corroborate previous studies that highlighted a sex‐specific association between AD and estrogen receptors. 15 , 16”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [16]
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Advances in Nanotechnology for Targeted Drug Delivery in Alzheimer's Disease
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- Authors
- Oveisgharan, S., Yang, J., Yu, L., Burba, D., Bang, W., Tasaki, S., Grodstein, F., Wang, Y., Zhao, J., De Jager, P. L., Schneider, J. A., & Bennett, D. A.
- Affiliations
- Rush University Medical Center (US)
- From the Rush Alzheimer's Disease Center (S.O., J.Y., L.Y., D.B., W.B., S.T., F.G., Y.W., J.A.S., D.A.B.), Rush University Medical Center, Chicago; Departments of Neurological Sciences (S.O., J.Y., L.Y., S.T., J.A.S., D.A.B.) and Internal Medicine (F.G.), Rush University Medical Center, Chicago, IL; Department of Epidemiology (J.Z.), University of Florida, Gainesville; Center for Translational & Computational Neuroimmunology (P.L.D.J.), Department of Neurology, Columbia University Irving Medical...
- ORCID
- Venue
- Neurology
- Published
- 2023-04-04
- Volume
- 100
- Issue
- 14
- Pages
- e1474-e1487
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC10104608
- OpenAlex
- W4318016632
- Cited by
- 53
- References
- 49
- Citations by year
- 2026: 10 · 2025: 20 · 2024: 16 · 2023: 7
- FWCI
- 9.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG017917, U01AG046152, R01AG015819, P30AG010161, R01AG064786, P30AG072975)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Menopause: Health Impacts and Treatments
- Keywords
- estrogen receptor gene, Alzheimer's disease, cognitive decline, G protein-coupled estrogen receptor, estrogen receptor 2, estrogen receptor 1, DNA methylation, gene expression, dorsolateral prefrontal cortex, tau tangles, amyloid plaques, sex differences, postmenopausal estrogen, genetic variants
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Humans, Male, Receptors, Estrogen, RNA, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Cognitive Dysfunction
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