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Researchers Discover How Alzheimer's Protein Behaves in Healthy Cells | Scientific American

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235 0 0 0 0 334 235 235 0 0 0 334 0 235 235 0 0 0 0-334ZM118 412a122 122 0 0 1 237 0 211 211 0 0 1-237 0Zm41-197a77 77 0 1 1 155 0 77 77 0 0 1-155 0Zm216 181c-14-43-48-77-91-92a101 101 0 1 0-96 0c-43 15-77 49-91 92a212 212 0 1 1 278 0Z"></path></svg><div class="dropdownIcon-XeKnP initials-z1adZ"></div></div></button></div></div></header><main class="main-gNG8x"><article class="article-GDG-h"><div class="article__header-bUswr article__header__reduce_padding_bottom-lno25"><div class="article_date_and_read_time-yLEUt"><p class="article_pub_date-EsKM-">December 6, 2001</p><p class="article_read_time-zEJJG">2<!-- --> min read</p></div><h1 class="article_hed-9vUZD"><p>Researchers Discover How Alzheimer's Protein Behaves in Healthy Cells</p></h1><div class="article_dek-bmjfm"><p></p></div><p class="article_authors-s5nSV">By <a class="article_authors__link--mMFB" href="/author/kristin-leutwyler/">Kristin Leutwyler</a> </p><div class="article_eyebrows-BqeOV"><div class="eyebrows_container-QeE5W 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type="submit">Sign Up</button></div></form></div><div class="body-n28ll prose-Yw0x0 prose-v4bYC article__body-ivA3W"><p class="" data-block="sciam/paragraph">Lawrence S. B. Goldstein and colleagues at the University of California in San Diego have now discovered how a protein involved in Alzheimer's disease&iquest;the amyloid precursor protein (APP)&iquest;normally behaves in the healthy brain cells of both mice and fruit flies. This information, published today in <i>Nature,</i> suggests an all new mechanism by which Alzheimer's might develop and thus opens new paths to explore towards potential therapies.</p><p class="" data-block="sciam/paragraph">The researchers focused on APP because it has long been known to degrade into so-called amyloid beta plaques, which are seen in the brains of Alzheimer's patients. What had remained mysterious was exactly how and where APP generates amyloid beta&iquest;and why that should lead to brain cell death. All cells in the body normally produce amyloid beta, Goldstein says, "that's why we asked what was special about neurons that made them susceptible to damage caused by APP."</p><p class="" data-block="sciam/paragraph">They found that APP plays an important role in moving signals through axons&iquest;the projections along which neurons communicate. In fruit flies, they showed that a lack of APP hindered the neurons' ability to send materials through axons. Too much APP clogged the axonal system and killed the neurons. These experiments appeared in <i>Neuron</i> last month. In the new report, they demonstrate in a mouse model that the transport system in question moves two enzymes&iquest;beta-secretase (Bace) and presenilin&iquest;that also seem to be responsible for breaking APP down into amyloid beta.</p><hr/><h2>On supporting science journalism</h2><p>If you&#x27;re enjoying this article, consider supporting our award-winning journalism by<!-- --> <a href="/getsciam/">subscribing</a>. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.</p><hr/><p class="" data-block="sciam/paragraph">"Once amyloid beta has been generated, it is possible that the axonal pathway becomes physically blocked," Goldstein says. "We're suggesting that with this blockage, a signal is generated saying that traffic is blocked and the neuron should die. Although this is only a first step in understanding the connection between APP, axonal transport and the location where amyloid beta is produced during disease, our work offers a possible approach for the eventual design of new Alzheimer's therapies that directly target amyloid beta and APP transport."</p></div><footer class="footer-u1I4n"><div class="divide-L7a-x"><div class="rights-Y0o9k"></div></div><div class="divide-L7a-x"></div><div class="divide-L7a-x"><div class="subdivide-5Zp4J"><a href="/author/kristin-leutwyler/">More by <span>Kristin Leutwyler</span></a></div></div><div class="divide-L7a-x"></div></footer><div class="breakoutContainer-8fsaw"><gpt-ad class="ad-G8iDN" unitpath="injector" style="--margin:0.25rem 0 1.25rem" id-format="gpt-unit-{}" sizes-from-0="320x450,300x250,300x50,320x50,fluid" sizes-from-745="320x450,728x90,300x250,fluid" sizes-from-1000="970x350,970x250,970x90,728x90,300x250,fluid" targeting-pos="article-footer"></gpt-ad></div></article></main><footer 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Goldstein and colleagues at the University of California in San Diego have now discovered how a protein involved in Alzheimer's disease驴the amyloid precursor protein (APP)驴normally behaves in the healthy brain cells of both mice and fruit flies. This information, published today in <i>Nature,</i> suggests an all new mechanism by which Alzheimer's might develop and thus opens new paths to explore towards potential therapies.</p>","why_box":"","content":[{"tag":"p","type":"paragraph","attributes":{},"content":"Lawrence S. B. Goldstein and colleagues at the University of California in San Diego have now discovered how a protein involved in Alzheimer's disease&iquest;the amyloid precursor protein (APP)&iquest;normally behaves in the healthy brain cells of both mice and fruit flies. This information, published today in <i>Nature,</i> suggests an all new mechanism by which Alzheimer's might develop and thus opens new paths to explore towards potential therapies."},{"tag":"p","type":"paragraph","attributes":{},"content":"The researchers focused on APP because it has long been known to degrade into so-called amyloid beta plaques, which are seen in the brains of Alzheimer's patients. What had remained mysterious was exactly how and where APP generates amyloid beta&iquest;and why that should lead to brain cell death. All cells in the body normally produce amyloid beta, Goldstein says, \\"that's why we asked what was special about neurons that made them susceptible to damage caused by APP.\\""},{"tag":"p","type":"paragraph","attributes":{},"content":"They found that APP plays an important role in moving signals through axons&iquest;the projections along which neurons communicate. In fruit flies, they showed that a lack of APP hindered the neurons' ability to send materials through axons. Too much APP clogged the axonal system and killed the neurons. These experiments appeared in <i>Neuron</i> last month. In the new report, they demonstrate in a mouse model that the transport system in question moves two enzymes&iquest;beta-secretase (Bace) and presenilin&iquest;that also seem to be responsible for breaking APP down into amyloid beta."},{"tag":"p","type":"paragraph","attributes":{},"content":"\\"Once amyloid beta has been generated, it is possible that the axonal pathway becomes physically blocked,\\" Goldstein says. \\"We're suggesting that with this blockage, a signal is generated saying that traffic is blocked and the neuron should die. Although this is only a first step in understanding the connection between APP, axonal transport and the location where amyloid beta is produced during disease, our work offers a possible approach for the eventual design of new Alzheimer's therapies that directly target amyloid beta and APP transport.\\""}],"authors":[{"mura_id":"5EF6269D-D002-4522-B4268A6012BDBFF0","url":"/author/kristin-leutwyler/","contentful_id":"UnMPMlVHnZosiqRY5x1kg","name":"Kristin 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