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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="2024-07-23T00:00:00-04:00" class="date-display-single">July 23, 2024</span></p><div class='syndicate'><h1>Gene variant slows form of inherited Alzheimer’s disease</h1><div class="callout callout-with-border"><h3>At a Glance</h3>
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<li>In a family with an inherited form of Alzheimer’s disease, those who carried a gene variant called <em>APOE3Ch</em> had a delay in cognitive impairment and dementia.</li>
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<li>More research is needed to see whether <em>APOE3Ch</em> has a protective effect in people beyond this family and to understand how it exerts its protective effect.</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="Brain tau levels">
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-large/public/news-events/research-matters/2024/nejmoa2308583_f1.jpg?itok=ZTTbzVIV&timestamp=1721744565 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/2024/nejmoa2308583_f1.jpg?itok=m3FAfyam&timestamp=1721744565 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/2024/nejmoa2308583_f1.jpg?itok=cOgC7-R-&timestamp=1721744565 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/2024/nejmoa2308583_f1.jpg?itok=uK-_zw8_&timestamp=1721744565 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/2024/nejmoa2308583_f1.jpg?itok=XU-eacN2&timestamp=1721744565 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/2024/nejmoa2308583_f1.jpg?itok=m3FAfyam&timestamp=1721744565" alt="Four tau PET brain images show larger areas of red in left two images" title="Brain tau levels" />
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</picture><span class="caption">Brain PET images reveal tau levels, with blue the lowest and red the highest. Left panels are from a typical person with the PSEN1 variant who had mild cognitive impairment. Right panels are from a person with the PSEN1 variant who also had one copy of the APOE3Ch variant.</span><span class="credit">Quiroz et al., NEJM</span></div>
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</div><p>Variations in certain genes can modify the risk of developing Alzheimer’s disease (AD) and other types of dementia. Some of the best understood variants to date are in a gene called <em>APOE</em>. This gene plays a role in the transport of cholesterol and other fatty molecules in the brain and body. People with a variant of <em>APOE</em> called <em>APOE4</em> have an increased risk of developing AD dementia. In contrast, people with a variant called <em>APOE2</em> appear to have some protection against developing dementia.</p>
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<p>In 2019, <a href="https://www.nih.gov/news-events/nih-research-matters/gene-variation-may-protect-against-alzheimers-disease">researchers found a hint</a> that a gene variant called <em>APOE3 Christchurch </em>(<em>APOE3Ch</em>) may also provide protection against the development of dementia. They had been following a woman from a family with an inherited variant in another gene called <em>PSEN1.</em> All other family members with this <em>PSEN1 </em>variant developed early-onset AD by middle age. But this woman, who had the <em>PSEN1 </em>variant and two copies of the <em>APOE3Ch</em> gene variant, remained cognitively healthy into her 70s.</p>
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|
||
<p>It wasn’t clear if having only one copy of <em>APOE3Ch</em> could also protect against cognitive decline in people with an AD-causing<em> PSEN1</em> mutation. In a new study, the researchers returned to the woman’s extended family of 1,077 people in Colombia. All were tracked with cognitive testing between 1995 and 2022.</p>
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<p>Led by Dr. Yakeel Quiroz from Massachusetts General Hospital, Dr. Francisco Lopera of the Grupo de Neurociencias de Antioquia in Medellín, Colombia, and Dr. Joseph Arboleda-Velasquez of Mass Eye and Ear, the research team compared the ages of cognitive impairment and dementia onset between family members with one copy of <em>APOE3Ch</em> and those without a copy of the potentially protective variant. Results from the new NIH-funded study were published on June 20, 2024, in the <em>New England Journal of Medicine</em>.</p>
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<p>Out of the 1,077 family members, 27 had one copy of <em>APOE3Ch</em>. After accounting for other factors that influence dementia risk, including sex, education level, and other variations in <em>APOE</em>, the people with one copy of<em> APOE3Ch</em> had some protection against dementia. They developed mild cognitive impairment—the precursor to dementia—an average of five years later (age 52) than relatives without the variant (age 47). They also met the criteria for dementia about four years later than expected (age 54 vs 50).</p>
|
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<p>The researchers conducted brain imaging on two of the participants. The scans revealed less buildup of tau protein tangles and preserved metabolic activity in brain regions associated with AD. Tau tangles are thought to contribute to the death of brain cells in AD. However, intriguingly, as seen in the first woman studied, the brains had high levels of amyloid-β plaque, another hallmark of AD.</p>
|
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<p>The team also looked at brain tissue samples taken at autopsy from four of the people with one copy of <em>APOE3Ch</em>. The blood vessels in these samples showed less damage than in people without <em>APOE3Ch</em>. Such damage has been linked to cognitive decline and dementia.</p>
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<p>“I am highly encouraged by our findings, as they suggest the potential for delaying cognitive decline and dementia in older individuals. Now we must leverage this new knowledge to develop effective treatments for dementia prevention,” Quiroz says.</p>
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<p>The team is now performing additional studies to understand the mechanisms through which <em>APOE3Ch</em> protects the brain. They are already taking advantage of the knowledge gained through study of this variant to design a therapy that shows promise in mouse models. Studies are also needed to measure whether <em>APOE3Ch</em> delays dementia in people who don’t carry a <em>PSEN1 </em>mutation.</p>
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<p>—by Sharon Reynolds</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-defines-major-genetic-form-alzheimer-s-disease" target="_top">Study Defines Major Genetic Form of Alzheimer’s Disease</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/research-context-diagnosing-dementia" target="_top">Research in Context: Diagnosing Dementia</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/alzheimer-s-tied-cholesterol-abnormal-nerve-insulation" target="_top">Alzheimer’s Tied to Cholesterol, Abnormal Nerve Insulation</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/common-drug-may-have-potential-treating-alzheimers-disease" target="_top">Common Drug May Have Potential for Treating Alzheimer’s Disease</a></li><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/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/gene-variation-may-protect-against-alzheimers-disease" target="_top">Gene Variation May Protect Against Alzheimer’s Disease</a></li><li><a href="https://www.nia.nih.gov/health/alzheimers-and-dementia" target="_top">Alzheimer’s and Dementia</a></li></ul><p class="footnote"><strong class="label-inline">References: </strong><a href="https://pubmed.ncbi.nlm.nih.gov/38899694/"><em>APOE3</em> Christchurch Heterozygosity and Autosomal Dominant Alzheimer's Disease.</a> Quiroz YT, Aguillon D, Aguirre-Acevedo DC, Vasquez D, Zuluaga Y, Baena AY, Madrigal L, Hincapié L, Sanchez JS, Langella S, Posada-Duque R, Littau JL, Villalba-Moreno ND, Vila-Castelar C, Ramirez Gomez L, Garcia G, Kaplan E, Rassi Vargas S, Ossa JA, Valderrama-Carmona P, Perez-Corredor P, Krasemann S, Glatzel M, Kosik KS, Johnson K, Sperling RA, Reiman EM, Sepulveda-Falla D, Lopera F, Arboleda-Velasquez JF. <em>N Engl J Med</em>. 2024 Jun 20;390(23):2156-2164. doi: 10.1056/NEJMoa2308583. PMID: 38899694.</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); Good Ventures; Remondi Family Foundation; Massachusetts General Hospital; Alzheimer’s Association; Banner Alzheimer’s Foundation; Werner Otto Foundation; German Federal Ministry of Education and Research; German Research Foundation; NOMIS Foundation.</p>
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