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首頁> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Luteinizing hormone modulates cognition and amyloid-deposition in Alzheimer APP transgenic mice
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Luteinizing hormone modulates cognition and amyloid-deposition in Alzheimer APP transgenic mice

機譯：黃體生成素調節阿爾茨海默病APP轉基因小鼠的認知和淀粉樣沉積

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Until recently, the study of hormonal influences in Alzheimer disease was limited to the role of sex steroids. Despite numerous epidemiological studies supporting a protective role for estrogen in Alzheimer disease, recent studies show that estrogen administration in elderly women increases the risk of disease. Reconciling these contradictory reports, we previously hypothesized that other hormones of the hypothalamic-pituitary-gonadal axis, such as luteinizing hormone, may be involved in the onset and development of the disease. In this regard, luteinizing hormone is elevated in Alzheimer disease and is known to modulate amyloidogenic processing of amyloid-beta protein precursor. Therefore, in this study, to evaluate the therapeutic potential of luteinizing hormone ablation, we administered a gonadotropin-releasing hormone analogue, leuprolide acetate, to an aged transgenic mouse model of Alzheimer disease (Tg 2576) and measured cognitive Y-maze performance and amyloid-beta deposition after 3 months of treatment. Our data indicate that luteinizing hormone ablation significantly attenuated cognitive decline and decreased amyloid-beta deposition as compared to placebo-treated animals. Importantly, leuprolide acetate-mediated reduction of amyloid-beta correlated with improved cognition. Since both cognitive loss and amyloid-beta deposition are features of Alzheimer disease, leuprolide acetate treatment may prove to be a useful therapeutic strategy for this disease. (C) 2006 Elsevier B.V. All rights reserved.
機譯：直到最近，激素對阿爾茨海默氏病影響的研究還僅限于性類固醇的作用。盡管許多流行病學研究支持雌激素在阿爾茨海默氏病中起保護作用，但最近的研究表明，老年婦女服用雌激素會增加患病的風險。為了調和這些矛盾的報道，我們先前假設下丘腦-垂體-性腺軸的其他激素（如黃體生成激素）可能與疾病的發作和發展有關。在這方面，促黃體生成激素在阿爾茨海默氏病中升高，并且已知其可調節淀粉樣β蛋白前體的淀粉樣生成過程。因此，在這項研究中，為了評估促黃體激素消融的治療潛力，我們向老年阿爾茨海默病轉基因小鼠模型（Tg 2576）施用了促性腺激素釋放激素類似物醋酸亮丙瑞林，并測量了認知Y迷宮性能和淀粉樣蛋白治療3個月后，β沉積。我們的數據表明，與安慰劑治療的動物相比，促黃體激素消融可顯著減輕認知能力下降并減少淀粉樣蛋白β沉積。重要的是，醋酸亮丙瑞林介導的淀粉樣β減少與認知能力提高有關。由于認知喪失和β淀粉樣蛋白沉積都是阿爾茨海默氏病的特征，醋酸亮丙瑞林治療可能被證明是該疾病的一種有用的治療策略。 （C）2006 Elsevier B.V.保留所有權利。

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