近日,，來自美國加州大學(xué)的研究人員發(fā)現(xiàn),，一種儲存在人類大腦中被認(rèn)為調(diào)控阿爾茨海默氏病發(fā)作的肽類物質(zhì)就像朊病毒一樣的方式發(fā)揮作用,，朊病毒是以通過哺乳動物神經(jīng)組織傳播方式發(fā)揮作用的,。這篇最新論文發(fā)表在PNAS雜志上,，研究人員證實β-淀粉樣肽（Aβ）會像朊病毒傳播方式那樣聚集到腦組織引起的疾病,。
朊病毒就是蛋白質(zhì)病毒,，是只有蛋白質(zhì)而沒有核酸的病毒,。朊病毒是一類能引起哺乳動物和人的中樞神經(jīng)系統(tǒng)病變的傳染性的病變因子，它們引起的疾病是傳染病如瘋牛病,。朊病毒對人類最大的威脅是可以導(dǎo)致人類和家畜患中樞神經(jīng)系統(tǒng)退化性病變,，最終不治而亡。
這項新的研究中,，科研人員使用熒光分子標(biāo)記β-淀粉樣蛋白后導(dǎo)入小鼠大腦中,，然后觀察近一年時間里小鼠大腦里發(fā)生的事件。由于帶有熒光分子,，研究人員能夠跟蹤肽的位置,，結(jié)果發(fā)現(xiàn)β-淀粉樣蛋白會傳播到大腦的另一側(cè)，最終破壞整個大腦結(jié)構(gòu),。這表明Aβ或許與朊病毒類似,，是一個可怕的東西。但β-淀粉樣蛋白會不會像朊病毒那樣具有傳染性,，迄今還沒有任何研究證實,。（生物谷：Bioon.com）
doi:10.1073/pnas.1206555109
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Purified and synthetic Alzheimer’s amyloid beta (Aβ) prions
Jan Sthra, Joel C. Wattsa, Zachary L. Mensinger, Abby Oehlerc, Sunny K. Grilloa, Stephen J. DeArmonda, Stanley B. Prusinera, and Kurt Gilesa
The aggregation and deposition of amyloid-β (Aβ) peptides are believed to be central events in the pathogenesis of Alzheimer’s disease (AD). Inoculation of brain homogenates containing Aβ aggregates into susceptible transgenic mice accelerated Aβ deposition, suggesting that Aβ aggregates are capable of self-propagation and hence might be prions. Recently, we demonstrated that Aβ deposition can be monitored in live mice using bioluminescence imaging (BLI). Here, we use BLI to probe the ability of Aβ aggregates to self-propagate following inoculation into bigenic mice. We report compelling evidence that Aβ aggregates are prions by demonstrating widespread cerebral β-amyloidosis induced by inoculation of either purified Aβ aggregates derived from brain or aggregates composed of synthetic Aβ. Although synthetic Aβ aggregates were sufficient to induce Aβ deposition in vivo, they exhibited lower specific biological activity compared with brain-derived Aβ aggregates. Our results create an experimental paradigm that should lead to identification of self-propagating Aβ conformations, which could represent novel targets for interrupting the spread of Aβ deposition in AD patients.
