阿爾茨海默�。ˋlzheimer’s disease,AD）是最常見(jiàn)的一種中樞神經(jīng)系統(tǒng)退行性疾病,1907年由德國(guó)精神科醫(yī)生Alois Alzheimer首先提出并以他的名字命名,AD以進(jìn)行性認(rèn)知功能障礙為特征,以神經(jīng)元間β淀粉樣蛋白（β-amyloid protein,Aβ）沉積形成老年斑,過(guò)磷酸化Tau蛋白為核心形成神經(jīng)元內(nèi)神經(jīng)纖維纏結(jié)（Neurofibrillary tangle,NFT）及特定腦區(qū)選擇性神經(jīng)元丟失和膠質(zhì)細(xì)胞過(guò)度炎癥反應(yīng),造成神經(jīng)元大量丟失,腦皮質(zhì)細(xì)胞減少,皮質(zhì)動(dòng)脈和小動(dòng)脈的血管發(fā)生淀粉樣變性為主要病理特征。據(jù)統(tǒng)計(jì),截止2016年全球有6630萬(wàn)人患癡呆,每年新增癡呆病例750萬(wàn)。隨著世界人口老齡化程度的不斷升高,AD的發(fā)病率也將不斷上升。我國(guó)的癡呆人數(shù)已近800萬(wàn),其中AD近600萬(wàn)。這將對(duì)家庭以致社會(huì)造成越來(lái)越沉重的負(fù)擔(dān),因此,對(duì)AD的致病機(jī)理及預(yù)防治療策略的研究顯得尤其迫切。值得指出的是多年大量研究中A?一直是構(gòu)成老年斑的核心成分,同時(shí)也被認(rèn)為是阿爾茨海默病最重要的致病物質(zhì)之一。關(guān)于AD的發(fā)病機(jī)制存在多種學(xué)說(shuō),包括氧化應(yīng)激學(xué)說(shuō)、Aβ級(jí)聯(lián)學(xué)說(shuō)、Tau蛋白假說(shuō)、... 

【文章來(lái)源】：河北醫(yī)科大學(xué)河北省

【文章頁(yè)數(shù)】：97 頁(yè)

【學(xué)位級(jí)別】：博士

【部分圖文】：

淫羊藿、黃芪、葛根有效成份組方對(duì)AD模型小鼠情景記憶的影響

圖 1-2 淫羊藿、黃芪、葛根有效成份組方對(duì) AD 模型小鼠 Aβ-42 分布的影響Fig.1-2 The IOD value showing the difference distribution of each groupAll data are expressed as the mean±SD. Intergroup differences were comparedwith multivariate analysis of variance followed by the least significantdifference test a. P <0.05 as each group vs C57 group; b. P<0.05 as eachgroup vs AD model group; c. P<0.05 as each group vs DFO group; d .P<0.05as each group vs Active compounds group; e. P<0.05 as each group vsEpimedium group; f. P < 0.05 as each group vs Astragaoside group; P < 0.05as each group vs Puerarin group..

1-3 淫羊藿、黃芪、葛根有效成份組方對(duì) AD 模型小鼠超微結(jié)構(gòu)的影響Fig.1-3 TEM showed the ultrastructural differences between each group C57 group mice, the neuronal ultrastructure was normal as exhibited byructure relatively normal, and organelles are relatively complete inorphology showing that the intact membranes, uniform cytoplasm, andomplete organelle structure. In APP/PS1 double transgenic AD model group,e nuclear shrinkaged and deformed, the mitochondrial cristae fused withartial membranes, rough endoplasmic reticulum degranulated, cytoplasmacuolization, mitochondria swelled and membrane ridges disappeared, whichere pointing out the damage of ultrastructure in neurons . The ultrastructuref Epimedium, Astragaoside , and Puerarin group were similar, presentingartial neural edema or loss normal morphology, the nuclear shrinkaged andeformed slightly, seldom mitochondria swelled and deformed or

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碩士論文
[1]LTD阻斷肽對(duì)于HU210在小鼠識(shí)別記憶影響上的作用[D]. 魏曉芳.陜西師范大學(xué) 2013
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