AI Article Synopsis
- Epidemiological studies show that women make up two-thirds of Alzheimer's disease cases, with menopause-related hormone drops as a potential risk factor, while decreasing testosterone in aging men may also heighten risk.
- Research indicates sex hormones like estradiol, progesterone, and testosterone have neuroprotective effects, but clinical trial results are inconsistent.
- The paper explores how mitochondria might play a role in the gender differences in Alzheimer's, and the link between the loss of sex hormones, mitochondrial dysfunction, and disease onset, potentially leading to new gender-specific treatments.
Article Abstract
Epidemiological studies revealed that two-thirds of Alzheimer's disease (AD) patients are women and the drop of sex steroid hormones after the menopause has been proposed to be one risk factor in AD. Similarly, the decrease of circulating testosterone levels with aging may also increase the risk of AD in men. Studies attest the neuroprotective effects of sex hormones in animal models of AD, but clinical trial data remain controversial. Here, we discuss the implication of mitochondria in gender differences observed in AD patients and animal models of AD. We summarize the role of mitochondria in aging and AD, pointing to the potential correlation between the loss of sex hormones and changes in the brain redox status. We discuss the protective effects of the sex hormones, estradiol, progesterone and testosterone with a specific focus on mitochondrial dysfunction in AD. The understanding of pathological processes linking the loss of sex hormones with mitochondrial dysfunction and mechanisms that initiate the disease onset may open new avenues for the development of gender-specific therapeutic approaches.
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| http://dx.doi.org/10.1016/j.neubiorev.2016.04.012 | DOI Listing |
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