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莫墨金蟲 (初入文壇)
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Autophagy, a process that takes part in the cell to degrade damaged organelles and misfolded or aggregated cytoplasmic proteins, comprises of mainly three processes: macroautophagy, microautophagy and chaperone-mediated autophagy, differing in the mode of delivery to the lysosome [47]. The last two processes are relatively unknown in contrast to macroautophagy in which two pathways to induce autophagy have been identified: mammalian target of rapamycin (mTOR)- dependent and mTOR-independent signaling pathways [48]. Failure in clearance mechanisms lead to the accumulation of defective protein (previously formed, misfolded and/or aggregated) which is a crucial hallmark in AD [30]. Clearance of defective proteins implicates the collaboration between molecular chaperones and targeted protein degradation (performed by proteasome-mediated degradation), chaperone-mediated autophagy (CMA) and selective macroautophagy [49]. A failing of misfolded protein removal leads to the building-up of aggregated deposits and the development of the pathogenesis of proteinopathies [50]. The evidences of abnormal protein dynamics due to defective degradation, produced by deficiency of the clearance systems, are overwhelming in AD. Cognitive improvements in different mouse models are studied in recent reports [19, 51]. Prior to mentioning degradation of defective proteins, there are also brain clearance mechanisms of A which follow two main routes [32], the direct way through the Blood-Brain Barrier (BBB), and the drainage via the interstitial fluid (ISF). The progressive impairment of these mechanisms, specially the first one leads, with the aging of the brain vessels, to the enhanced formation of CAA, affecting leptomeningeal arteries, cortical arteries and capillaries [33]. 相關(guān)專業(yè)：藥學(xué)，分子生物學(xué) 有效期：2014年8月11-2014年8月12日 謝謝！ |
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| 自噬是在細(xì)胞中參與受損細(xì)胞器的降解，以及降解細(xì)胞質(zhì)中錯(cuò)誤折疊或聚集蛋白質(zhì)的過程，主要包括三個(gè)過程：巨自噬、微自噬和分子伴侶介導(dǎo)的自噬，其差別在于運(yùn)輸至溶酶體的模式不同[47]。與巨自噬相比，人們對(duì)微自噬和分子伴侶介導(dǎo)的自噬的了解還很有限。但就巨自噬而言，目前已經(jīng)發(fā)現(xiàn)了兩條信號(hào)通路可以誘導(dǎo)巨自噬：即mTOR依賴性和非依賴性信號(hào)途徑[48]。清除機(jī)制失敗可以引起缺陷蛋白質(zhì)（以前形成的，錯(cuò)誤折疊和/或聚集）的累積，而這正是阿爾茨海默�。ˋD）的一個(gè)重要標(biāo)志[30]。對(duì)缺陷蛋白質(zhì)的清除需要分子伴侶和目標(biāo)蛋白質(zhì)的降解（蛋白酶體介導(dǎo)的降解）、分子伴侶介導(dǎo)的自噬（CMA）、以及選擇性巨自噬之間的協(xié)作[49]。如果錯(cuò)誤折疊蛋白清除失敗，就會(huì)導(dǎo)致缺陷蛋白逐漸集聚，引發(fā)相應(yīng)的蛋白質(zhì)病癥[50]。在阿爾茨海默病中，有大量證據(jù)表明，由于清除機(jī)制的缺陷造成對(duì)缺陷蛋白質(zhì)的清除障礙，可以引起蛋白質(zhì)動(dòng)力學(xué)異常。最近在不同小鼠模型的研究報(bào)告表明，認(rèn)知能力有所改善[19，51]。在動(dòng)用這些對(duì)缺陷蛋白質(zhì)的降解機(jī)制之前，大腦也有其清除機(jī)制，主要包括兩個(gè)主要途徑[32]：一是直接通過血腦屏障（BBB）清除，二是通過組織間液（ISF）的排放。隨著這些機(jī)制出現(xiàn)漸進(jìn)性障礙，特別是隨腦血管老化引起的第一個(gè)機(jī)制（即直接通過BBB）障礙，引起淀粉樣腦血管疾病（CAA）的加速形成，影響軟腦膜動(dòng)脈，皮質(zhì)動(dòng)脈和毛細(xì)血管[33]。 |
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