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<h2 class="element-invisible">You are here</h2><div class="breadcrumb"><a href="/">Home</a> » <a href="/news-events">News & Events</a> » <a href="/news-events/nih-research-matters">NIH Research Matters</a></div> <div class="l-region l-region--section-header">
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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2022-12-06T00:00:00-05:00" class="date-display-single">December 6, 2022</span></p><div class='syndicate'><h1>Alzheimer’s tied to cholesterol, abnormal nerve insulation </h1><div class="callout callout-with-border"><h3>At a Glance</h3>
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<li>Researchers found evidence that the Alzheimer’s-related gene <em>APOE4</em> disrupts cholesterol management in the brain and weakens insulation around nerve fibers.</li>
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<li>A drug that affects cholesterol led to improved learning and memory in mice with the gene, pointing to a potential new approach for treating dementia in Alzheimer’s disease.</li>
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</ul></div><div class="media-float-right"><div class="ds-1col file file-image file-image-jpeg view-mode-floated_media clearfix">
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<picture title="Illustration of various cells within the brain">
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<!--[if IE 9]><video style="display: none;"><![endif]-->
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-large/public/news-events/research-matters/2022/20221206-ad.jpg?itok=jNZ0kvEt&timestamp=1670338113 1x" media="screen and (min-width: 960px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium/public/news-events/research-matters/2022/20221206-ad.jpg?itok=n4PNvwnY&timestamp=1670338113 1x" media="screen and (min-width: 800px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium-small/public/news-events/research-matters/2022/20221206-ad.jpg?itok=9GLRG9sW&timestamp=1670338113 1x" media="screen and (min-width: 600px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-small/public/news-events/research-matters/2022/20221206-ad.jpg?itok=zBgd653k&timestamp=1670338113 1x" media="screen and (min-width: 480px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-tiny/public/news-events/research-matters/2022/20221206-ad.jpg?itok=2mf0igqO&timestamp=1670338113 1x" media="screen and (min-width: 0)" />
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<!--[if IE 9]></video><![endif]-->
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<img src="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium/public/news-events/research-matters/2022/20221206-ad.jpg?itok=n4PNvwnY&timestamp=1670338113" alt="Illustration of various cells within the brain" title="Illustration of various cells within the brain" />
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</picture><span class="caption">Cells of the brain include oligodendrocytes (on right in grey), which make fatty myelin sheaths that surround long nerve fibers. </span><span class="credit">Juan Gaertner / Shutterstock</span></div>
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</div><p>The protein apolipoprotein E (APOE) plays a key role throughout the body. It helps to transport cholesterol and other fatty molecules, or lipids. The gene that produces APOE comes in a few different varieties. The most common is called <em>APOE3.</em></p>
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<p>The most notorious is <em>APOE4, </em>which has long been linked to an increased risk of dementia in Alzheimer’s disease<em>. </em>People who inherit one copy of the <em>APOE4 </em>gene have up to a fourfold greater risk of developing Alzheimer’s disease dementia. Inheriting two copies of <em>APOE4 </em>elevates the risk up to twelvefold. But despite years of study, scientists have little understanding of how <em>APOE4</em> affects the human brain and boosts dementia risk.</p>
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||
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<p><a href="https://www.nih.gov/news-events/nih-research-matters/study-reveals-how-apoe4-gene-may-increase-risk-dementia">Earlier research</a> by Dr. Li-Huei Tsai of the Massachusetts Institute of Technology and others found that <em>APOE4</em> might raise Alzheimer’s risk by altering lipid metabolism in certain brain cells. But the underlying details of the process remained unclear.</p>
|
||
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||
<p>To build on these findings, the team conducted a multi-pronged study that assessed gene activity of all major cell types in post-mortem human brain tissue from 32 men and women who had one, two, or no copies of the <em>APOE4 </em>gene. Results were published in <em>Nature</em> on November 24, 2022.</p>
|
||
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||
<p>The researchers found that <em>APOE4</em> affected gene expression across all measured cell types. The team then took a closer look at genes related to cholesterol and other lipids. Cholesterol-manufacturing genes were overly expressed, and cholesterol-transporting genes dysregulated, in brain cells called oligodendrocytes with the <em>APOE4 </em>gene. Oligodendrocytes are found in the brain and spinal cord. They make and maintain a fatty substance called myelin that surrounds and insulates long nerve fibers. The abnormalities were more extreme in oligodendrocytes with two copies of <em>APOE4</em> rather than one.</p>
|
||
|
||
<p>To better understand how <em>APOE4 </em>affects oligodendrocytes, the scientists created laboratory cultures of the cells with and without the <em>APOE4</em> gene. Oligodendrocytes with <em>APOE4 </em>tended to accumulate abnormal amounts of cholesterol within their cells, rather than using it to make healthy myelin sheaths around nerve fibers. When the scientists examined post-mortem human brains, they noted that myelin sheaths tended to be fewer and thinner in brains that carried the <em>APOE4 </em>gene.</p>
|
||
|
||
<p>The scientists next used model systems to test whether <em>APOE4-</em>related abnormalities might be reversed via drugs that affect cholesterol processing. They found that a drug called cyclodextrin, which promotes cholesterol transport, reduced cholesterol buildup and improved myelin sheath formation in cultured oligodendrocytes. It did the same in mice with two copies of <em>APOE4. </em>The mice also performed slightly better in learning and memory tasks after treatment with the drug.</p>
|
||
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||
<p>These findings open new avenues for exploring the underlying mechanisms of Alzheimer’s disease dementia and for designing potential therapeutics.</p>
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||
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||
<p>“It’s encouraging that we’ve seen a way to rescue oligodendrocyte function and myelination in lab and mouse models,” Tsai says. “I feel that lipid dysregulation could be very fundamental biology underlying a lot of the pathology we observe.”</p>
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<p>—by Vicki Contie</p></div><h2 class="label-above">Related Links</h2><ul class="spaced print-urls"><li><a href="https://www.nih.gov/news-events/nih-research-matters/study-reveals-how-apoe4-gene-may-increase-risk-dementia" target="_top">Study Reveals How APOE4 Gene May Increase Risk for Dementia</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/immune-cells-control-waste-clearance-brain" target="_top">Immune Cells Control Waste Clearance in the Brain</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/blood-tests-show-promise-early-alzheimers-diagnosis" target="_top">Blood Tests Show Promise for Early Alzheimer’s Diagnosis</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/gene-expression-signatures-alzheimers-disease" target="_top">Gene Expression Signatures of Alzheimer’s Disease</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/early-epigenetic-effects-alzheimers-disease" target="_top">Early Epigenetic Effects in Alzheimer’s Disease</a></li><li><a href="https://newsinhealth.nih.gov/special-issues/seniors/dealing-dementia" target="_top">Dealing with Dementia</a></li><li><a href="https://www.nia.nih.gov/health/alzheimers" target="_top">Alzheimer's Disease & Related Dementias</a></li><li><a href="https://www.nia.nih.gov/health/alzheimers-disease-genetics-fact-sheet" target="_top">Alzheimer's Disease Genetics Fact Sheet</a></li><li><a href="https://www.alzheimers.gov/" target="_top">Alzheimers.gov</a></li></ul><p class="footnote"><strong class="label-inline">References: </strong><a href="https://pubmed.ncbi.nlm.nih.gov/36385529/">APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes.</a> Blanchard JW, Akay LA, Davila-Velderrain J, von Maydell D, Mathys H, Davidson SM, Effenberger A, Chen CY, Maner-Smith K, Hajjar I, Ortlund EA, Bula M, Agbas E, Ng A, Jiang X, Kahn M, Blanco-Duque C, Lavoie N, Liu L, Reyes R, Lin YT, Ko T, R'Bibo L, Ralvenius WT, Bennett DA, Cam HP, Kellis M, Tsai LH. <em>Nature.</em> 2022 Nov; 611(7937):769-779. doi: 10.1038/s41586-022-05439-w. Epub 2022 Nov 16. PMID: 36385529.</p><p class="footnote"><strong class="label-inline">Funding: </strong>: NIH’s National Institute on Aging (NIA) and National Institute of Neurological Disorders and Stroke (NINDS); Robert A. and Renee E. Belfer Family; JPB Foundation; Carol and Gene Ludwig Family Foundation, Cure Alzheimer’s Fund.</p>
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