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Molecular and cellular mechanisms of sporadic Alzheimer's disease: Studies on rodent models in vivo

机译:散发性阿尔茨海默病的分子与细胞机制:体内啮齿动物模型的研究

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摘要

In this review, recent data are presented on molecular and cellular mechanisms of pathogenesis of the most widespread (about 95%) sporadic forms of Alzheimer's disease obtained on in vivo rodent models. Although none of the available models can fully reproduce the human disease, several key molecular mechanisms (such as dysfunction of neurotransmitter systems, especially of the acetylcholinergic system, beta-amyloid toxicity, oxidative stress, neuroinflammation, mitochondrial dysfunction, disturbances in neurotrophic systems) are confirmed with different models. Injection models, olfactory bulbectomy, and senescence accelerated OXYS rats are reviewed in detail. These three approaches to in vivo modeling of sporadic Alzheimer's disease have demonstrated a considerable similarity in molecular and cellular mechanisms of pathology development. Studies on these models provide complementary data, and each model possesses its specific advantages. A general analysis of the data reported for the three models provides a multifaceted and the currently most complete molecular picture of sporadic Alzheimer's disease. This is highly relevant also from the practical viewpoint because it creates a basis for elaboration and preclinical studies of means for treatment of this disease.
机译:在该审查中,近期数据显示了在体内啮齿动物模型中获得的最广泛(约95%)散发形式的阿尔茨海默病的散发形式的分子和细胞机制。虽然没有任何可用的模型可以完全繁殖人类疾病,但是几个关键的分子机制(例如神经递质系统的功能障碍,尤其是乙酰胆碱能系统,β-淀粉样毒性,氧化应激,神经肾性炎症,线粒体功能障碍,神经营养系统的干扰)是用不同的型号确认。详细审查注射模型,嗅到血症植物和衰老加速的oxys大鼠。这三种在孢子症阿尔茨海默病的体内建模方法已经证明了病理发育的分子和细胞机制方面具有相当大的相似性。这些模型的研究提供了互补数据,每个模型都具有其特定的优势。对三种模型报告的数据的一般分析提供了零孢素阿尔茨海默病的多方面和目前最完整的分子图片。这也来自实际观点,这是高度相关的,因为它为治疗这种疾病的手段创造了阐述和临床前研究的基础。

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