Estrogen-replacement therapy and Alzheimer's disease in the Italian Longitudinal Study on Aging

Abstract

Our data from a population-based study support the hypothesis that estrogen-replacement therapy is associated with a reduced prevalence of Alzheimer's disease in postmenopausal women. Prospective clinical trials are required to enable women and their physicians to weigh risks and benefits of estrogen-replacement therapy for the prevention of dementia.

Effects of estrogen on lifespan and motor functions in female hSOD1 G93A transgenic mice

“…Estrogen exerts many diverse cellular effects in neural tissue, including acting as a neurotrophic factor during the processes of cell proliferation and differentiation. Estrogen also exerts neuroprotective effects in pathological environments, including glutamate excitotoxicity [26], oxidative stress [27,28], β-amyloid-induced toxicity [26], neurotoxin treatment [29], cerebral ischemia [30][31][32], forebrain transections [33], excitotoxin-induced forebrain injury [34][35][36], Alzheimer's disease [37][38][39], and Parkinson's disease [40].…”

Preliminary evidence that estrogen protects against age-related hippocampal atrophy

“…A number of studies have examined cognitive performance, particularly memory performance, in postmenopausal women, and have reported a beneficial effect of ERT [29,31,[46][47][48]. While there are some conflicting findings, especially with regard to the use of estrogen for the treatment of AD, a growing body of evidence indicates that ERT reduces the risk of AD in postmenopausal women [1,2,5,7,21,23,32,41,56].…”

Diabetes, sugar-coated but harmful to the brain

“…However, epidemiological studies have to be interpreted carefully. Two epidemiological studies had reported that estrogen hormone replacement therapy [17] or use of nonsteroidal anti-inflammatory [18] may protect against dementia, whereas no such effects were found in prospective treatment studies [19;20]. Although in experimental rat models, the spontaneous onset of T2DM is associated with betaamyloid and phospho-tau accumulation as well as neurite degeneration and neuronal loss [21], we have to bear in mind that the physiology of the rodent is very different than that of the human.…”