Why Women Have More Alzheimer's Disease Than Men: Gender and Mitochondrial Toxicity of Amyloid-β Peptide
Open accessAbstract
The main risk factors for developing Alzheimer's disease (AD) are age and gender. The incidence of the disease is higher in women than in men, and this cannot simply be attributed to the higher longevity of women versus men. Thus, there must be a specific pathogenic mechanism to explain the higher incidence of AD cases in women. In this regard, it is notable that mitochondria from young females are protected against amyloid-beta toxicity, generate less reactive oxygen species, and release less apoptogenic signals than those from males. However, all this advantage is lost in mitochondria from old females. Since estrogenic compounds protect against mitochondrial toxicity of amyloid-beta, estrogenic action may be important in protecting cells from amyloid-beta toxicity and suggests a possible treatment or prevention strategy for AD. Unfortunately, to date, clinical trials with Ginkgo biloba and other estrogenic therapies have not proved successful in treating AD. As such, more experiments and clinical trials are indeed warranted to find conditions in which estrogenic compounds may be useful to prevent or treat AD.
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In women, intact mitochondrial function protects individuals against Aβ toxicity, probably due to estrogen-mediated suppression of ROS and apoptogenic signals.
“In women, intact mitochondrial function protects individuals against Aβ toxicity probably due to estrogen-mediated suppression in ROS and apoptogenic signals generated in women [58].”
From Sex specific molecular networks and key drivers of Alzheimer’s disease (2023) · cites this paper as [58]
The sections on female mitochondria and estrogenic compounds report that mitochondria from young female rats are protected against Aβ toxicity and that estrogens reduce mitochondrial peroxide release. The copy does not establish this protection for women generally—older female rat mitochondria were not protected—or identify suppression of apoptogenic signals as its mechanism. No page numbers were supplied for these passages. (LLM, conf=0.86)
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- Authors
- Viña, J., & Lloret, A.
- Affiliations
- Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain
- Universitat de València (ES)
- ORCID
- Lloret, Ana
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2010-06-03
- Volume
- 20
- Issue
- s2
- Pages
- S527-S533
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2128969673
- Cited by
- 447
- References
- 4
- Citations by year
- 2026: 12 · 2025: 24 · 2024: 51 · 2023: 33 · 2022: 42 · 2021: 44 · 2020: 44 · 2019: 36 · 2018: 43 · 2017: 27 · 2016: 21 · 2015: 18 · 2014: 15 · 2013: 14 · 2012: 15
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Alzheimer s Disease (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, sex differences
- MeSH terms
- Alzheimer Disease, Estrogens, Female, Humans, Male, Mitochondria, Models, Biological, Risk Factors, Sex Characteristics, Up-Regulation, Amyloid beta-Peptides
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