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<meta name="keywords" content="Alzheimer’s, dementia, APOE, APOE4, APOE ε4, lipid transport, lipid homeostasis, choline, phospholipids, lipidomics, induced pluripotent stem cells, astrocytes, Li-Huei Tsai, Susan Lindquist, Science Translational Medicine." />
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<div about="/news-events/nih-research-matters/study-reveals-how-apoe4-gene-may-increase-risk-dementia" typeof="sioc:Item foaf:Document" class="ds-1col node node--nih-research-matters view-mode-full node--full node--nih-research-matters--full clearfix">
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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2021-03-16T00:00:00-04:00" class="date-display-single">March 16, 2021</span></p><div class='syndicate'><h1>Study reveals how APOE4 gene may increase risk for dementia</h1><div class="callout callout-with-border"><h3>At a Glance</h3>
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<li>Researchers found that the <em>APOE4</em> gene may increase the risk of developing Alzheimer’s disease and other dementias by altering brain cells’ lipid metabolism. </li>
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<li>Choline supplements reversed these defects in cell studies, supporting further research in people carrying <em>APOE4</em>.</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="Neurons with amyloid plaques">
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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/2021/20210316-plaque.jpg?itok=ViItha6m&timestamp=1615901239 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/2021/20210316-plaque.jpg?itok=Yakdw6UK&timestamp=1615901239 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/2021/20210316-plaque.jpg?itok=iJdo9hcd&timestamp=1615901239 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/2021/20210316-plaque.jpg?itok=rwzQGqOz&timestamp=1615901239 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/2021/20210316-plaque.jpg?itok=K8pzPaBR&timestamp=1615901239 1x" media="screen and (min-width: 0)" />
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<img src="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium/public/news-events/research-matters/2021/20210316-plaque.jpg?itok=Yakdw6UK&timestamp=1615901239" alt="Neurons with amyloid plaques" title="Neurons with amyloid plaques" />
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</picture><span class="caption">The study suggests that dementia may be caused by lipid imbalances in brain cells. This illustration shows neurons with amyloid plaques, a hallmark of Alzheimer’s disease, in yellow. </span><span class="credit">selvanegra / iStock / Getty Images Plus</span></div>
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</div><p>Certain genes can increase the risk of developing dementia, including Alzheimer’s disease. One of the most significant genetic risk factors is a form of the <em>apolipoprotein E</em> gene called <em>APOE4</em>. About 25% of people carry one copy of <em>APOE4</em>, and 2 to 3% carry two copies. <em>ApoE4</em> is the strongest risk factor gene for Alzheimer’s disease, although inheriting <em>ApoE4</em> does not mean a person will definitely develop the disease.</p>
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<p>The <em>APOE </em>gene comes in several different forms, or alleles. <em>APOE3</em> is the most common and not believed to affect Alzheimer’s risk. <em>APOE2</em> is relatively rare and may provide some protection against Alzheimer’s disease.</p>
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<p>The reason <em>APOE4</em> increases Alzheimer’s risk isn’t not well understood. The APOE protein helps carry cholesterol and other types of fat in the bloodstream. Recent studies suggest that problems with brain cells’ ability to process fats, or lipids, may play a key role in Alzheimer’s and related diseases.</p>
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<p>Lipid imbalances can impair many of a cell’s essential processes. This includes creating cell membranes, moving molecules within the cell, and generating energy.</p>
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<p>Dr. Li-Huei Tsai and the late Dr. Susan Lindquist of MIT investigated how <em>APOE4</em> affects lipid metabolism in brain cells. The study was funded by NIH’s National Institute on Aging (NIA), National Cancer Institute (NCI), and National Institute of Neurological Disorders and Stroke (NINDS). Dr. Priyanka Narayan of NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) was a co-first author. Findings were published in <em>Science Translational Medicine </em>on March 3, 2021.</p>
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||
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||
<p>The research team began by creating brain cells called astrocytes using stem cells. They used skin cells from people carrying <em>APOE3</em> or <em>APOE4</em> that were reprogrammed into a state where they could develop into any cell. Called induced pluripotent stem cells, these cells were then coaxed into becoming astrocytes, star-shaped cells that produce the most ApoE in the brain.</p>
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<p>The researchers found changes in how <em>APOE4</em> astrocytes were able to process lipids. The astrocytes accumulated droplets containing fats called triglycerides. These triglycerides had many more unsaturated fatty acid chains than normal. Lipid buildup in the <em>APOE4</em> astrocytes was much greater than in <em>APOE3</em> astrocytes. The researchers also found disruptions in lipid metabolism when they coaxed the cells into becoming other brain cells called microglia.</p>
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<p>The team next tested whether yeast cells with the human version of <em>APOE4</em> would have the same disruption in lipid metabolism. Lipid metabolism pathways are very similar between yeast and humans. Yeast with a copy of the <em>APOE4</em> gene accumulated lipids much like the human cells did. Genetic screens in the yeast identified a molecular pathway that could be responsible for the defects. Boosting the activity of a pathway that normally produces phospholipids—an essential building block of the cell membrane—reversed some of the lipid accumulation.</p>
|
||
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||
<p>Further research showed that supplementing the yeast cells’ culture with choline restored normal lipid metabolism. Choline is needed to synthesize phospholipids. Similar benefits were seen after treating the human <em>APOE4</em> astrocyte cells with choline. These findings provide preliminary support for testing choline supplements in people who carry <em>APOE4</em>.</p>
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||
<p>“What we would really like to see is whether in the human population, in those <em>APOE4</em> carriers, if they take choline supplements to a sufficient amount, whether that would delay or give them some protection against developing dementia or Alzheimer's disease,” Tsai says.</p>
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<p>However, it is important to keep in mind that results from isolated cells don’t often translate into successful approaches when tested in people.</p>
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<p>—by Erin Bryant</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/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/new-blood-test-method-may-predict-alzheimers-disease" target="_top">New Blood Test Method May Predict Alzheimer's Disease</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/alzheimers-gene-contributes-blood-brain-barrier-breakdown" target="_top">Alzheimer’s Gene Contributes to Blood-Brain Barrier Breakdown</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/predicting-alzheimers-disease-progression" target="_top">Predicting Alzheimer’s Disease Progression</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/gene-variation-may-protect-against-alzheimers-disease" target="_top">Gene Variation May Protect Against Alzheimer’s Disease</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://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.ninds.nih.gov/Disorders/All-Disorders/Alzheimers-Disease-Information-Page" target="_top">Alzheimer's Disease Information Page</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.nia.nih.gov/health/alzheimers-disease-research-centers" target="_top">Alzheimer's Disease Research Centers</a></li></ul><p class="footnote"><strong class="label-inline">References: </strong><a href="https://pubmed.ncbi.nlm.nih.gov/33658354/"><em>APOE4</em> disrupts intracellular lipid homeostasis in human iPSC-derived glia.</a> Sienski G, Narayan P, Bonner JM, Kory N, Boland S, Arczewska AA, Ralvenius WT, Akay L, Lockshin E, He L, Milo B, Graziosi A, Baru V, Lewis CA, Kellis M, Sabatini DM, Tsai LH, Lindquist S. <em>Sci Transl Med.</em> 2021 Mar 3;13(583):eaaz4564. doi: 10.1126/scitranslmed.aaz4564. PMID: 33658354.</p><p class="footnote"><strong class="label-inline">Funding: </strong>NIH’s National Institute on Aging (NIA), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Cancer Institute (NCI), and National Institute of Neurological Disorders and Stroke (NINDS); Howard Hughes Medical Institute; Neurodegeneration Consortium; Robert A. and Renee E. Belfer Foundation; Ludwig Family Foundation; Kara and Stephen Ross.</p>
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