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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2020-05-12T00:00:00-04:00" class="date-display-single">May 12, 2020</span></p><div class='syndicate'><h1>Alzheimer’s gene contributes to blood-brain barrier breakdown</h1><div class="callout callout-with-border"><h3>At a Glance</h3>
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<li>Damage to the blood-brain barrier may contribute to the development of Alzheimer’s dementia in people carrying a high-risk gene variation.</li>
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<li>Developing drugs to protect blood-brain barrier cells may help prevent or treat the disease in people with this gene.</li>
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-large/public/news-events/news-releases/2020/20200512-mri.jpg?itok=5uduk5ed&timestamp=1589289822 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/news-releases/2020/20200512-mri.jpg?itok=T3NKVgqT&timestamp=1589289822 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/news-releases/2020/20200512-mri.jpg?itok=sAjKmx6e&timestamp=1589289822 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/news-releases/2020/20200512-mri.jpg?itok=UnYltUU0&timestamp=1589289822 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/news-releases/2020/20200512-mri.jpg?itok=dxYcWu5Y&timestamp=1589289822 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/news-releases/2020/20200512-mri.jpg?itok=T3NKVgqT&timestamp=1589289822" alt="Person getting a brain scan" title="Person getting a brain scan" />
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</picture><span class="caption">Researchers investigated whether the blood-brain barrier may contribute to development of Alzheimer’s dementia in people carrying a high-risk gene variation. </span><span class="credit">alvarez / E+ via Getty Images</span></div>
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</div><p>Alzheimer’s disease is the most common cause of dementia in older adults. Brain changes associated with the disease include abnormal clumps (amyloid-β plaques) and tangled bundles of fibers (tau tangles). It’s thought that these changes eventually cause the death of nerve cells, leading to a progressive decline in memory and thinking skills.</p>
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<p>But amyloid-β and tau are likely not the only drivers of Alzheimer’s dementia. Recent studies suggest that breakdown of the blood-brain barrier may also play a role. The blood-brain barrier is a protective, tightly packed mix of cells that sits between the blood vessels that lead to the brain and the brain tissue itself.</p>
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<p>People with a variation of the gene <em>apolipoprotein E</em> (<em>APOE</em>), called <em>APOE4,</em> have an increased risk of developing Alzheimer’s dementia, often at an earlier age. <em>APOE4</em> is known to contribute to amyloid-β and tau accumulation. A research team led by Drs. Axel Montagne and Berislav Zlokovic from the University of Southern California wanted to know if <em>APOE4</em> also affects the blood-brain barrier.</p>
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<p>The researchers recruited 245 older adults to undergo a type of brain imaging called dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). DCE-MRI can identify leakiness in the blood-brain barrier. Study participants also underwent measurements of amyloid-β and tau, and of cognitive function over time.</p>
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<p>The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Neurological Disorders and Stroke (NINDS). Results were published on May 7, 2020, in <em>Nature</em>.</p>
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<p>Out of the 245 participants, 101 carried one or two copies of the high-risk <em>APOE4</em> gene variation, and 144 had <em>APOE3</em>, a normal variation of the gene. On imaging, people with <em>APOE4</em> had increased breakdown of the blood-brain barrier in two areas of the brain important for memory and cognition.</p>
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<p>This breakdown was worse in people with <em>APOE4</em> who were already experiencing mild cognitive decline. These patients had not yet experienced a loss of brain tissue. This suggests that breakdown of the blood-brain barrier may occur early in the course of the disease.</p>
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<p>The breakdown in the blood-brain barrier also occurred apart from amyloid-β and tau levels measured in participants’ cerebrospinal fluid or brain, suggesting it may contribute independently to cognitive impairment and dementia.</p>
|
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<p>Previous research suggested that cells called pericytes, which help maintain the blood-brain barrier, may become damaged in people with <em>APOE4</em>. The researchers measured levels of a protein that reflects pericyte damage in 146 participants at the start of the study who then had their cognitive function tracked.</p>
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<p>The people with <em>APOE4</em> and more pericyte damage were more likely to experience cognitive decline during the study (up to 4.5 years). Pericyte damage predicted cognitive decline independently of amyloid-β and tau levels in the people with <em>APOE4</em>. No such relationship was found in people with the <em>APOE3</em> variation.</p>
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||
<p>Further work identified a specific inflammatory pathway associated with pericyte injury that was more active in <em>APOE4</em> carriers. Lab experiments showed that ApoE4 secreted by pericytes activated this pathway in nearby pericytes. ApoE3 did not. Blocking this pathway in mice carrying <em>APOE4</em> protected the blood-brain barrier and preserved brain function.</p>
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<p>“Our findings suggest that breakdown of the blood-brain barrier contributes to the cognitive decline associated with <em>APOE4</em> and may be a target for the development of preventive or therapeutic drugs for people who carry this gene variation,” Zlokovic says.</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/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/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/mediterranean-diet-may-slow-development-alzheimers-disease" target="_top">Mediterranean Diet May Slow Development of Alzheimer’s Disease</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/sleep-deprivation-increases-alzheimers-protein" target="_top">Sleep Deprivation Increases Alzheimer’s Protein</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></ul><p class="footnote"><strong class="label-inline">References: </strong><a href="https://www.ncbi.nlm.nih.gov/pubmed/32376954">APOE4 leads to blood-brain barrier dysfunction predicting cognitive decline.</a> Montagne A, Nation DA, Sagare AP, Barisano G, Sweeney MD, Chakhoyan A, Pachicano M, Joe E, Nelson AR, D'Orazio LM, Buennagel DP, Harrington MG, Benzinger TLS, Fagan AM, Ringman JM, Schneider LS, Morris JC, Reiman EM, Caselli RJ, Chui HC, Tcw J, Chen Y, Pa J, Conti PS, Law M, Toga AW, Zlokovic BV. <em>Nature</em>. 2020 May;581(7806):71-76. doi: 10.1038/s41586-020-2247-3. Epub 2020 Apr 29. PMID: 32376954.</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); Alzheimer’s Association; Cure Alzheimer’s Fund; Foundation Leducq Transatlantic Network of Excellence for the Study of Perivascular Spaces in Small Vessel Disease; Open Philanthropy; L. K. Whittier Foundation; State of Arizona; Avid Radiopharmaceuticals.</p>
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