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<meta name="DC.Title" content="APOE*E4 Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline" />
<meta name="DC.Identifier" content="10.3174/ajnr.A5184" />
<meta name="DC.Date" content="2017-07-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
<meta name="DC.Rights" content="© 2017 by American Journal of Neuroradiology. Indicates open access to non-subscribers at www.ajnr.org" />
<meta name="DC.AccessRights" content="open-access" />
<meta name="DC.Description" content="BACKGROUND AND PURPOSE: The presence of apolipoprotein E4 ( APOE * E4 ) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of APOE * E4 on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.

MATERIALS AND METHODS: This prospective study included 382 community-dwelling elderly controls. At baseline, participants underwent MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel-based morphometry and ROI analysis of GM.

RESULTS: APOE * E4 -related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no APOE * E4- related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.

CONCLUSIONS: APOE * E4 -related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, APOE * E4 status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.

AD
:   Alzheimer disease
APOE 
:   apolipoprotein E 
dCON
:   cognitively deteriorating controls
MCI
:   mild cognitive impairment
sCON
:   cognitively stable controls" />
<meta name="DC.Contributor" content="S. Haller" />
<meta name="DC.Contributor" content="M.-L. Montandon" />
<meta name="DC.Contributor" content="C. Rodriguez" />
<meta name="DC.Contributor" content="M. Ackermann" />
<meta name="DC.Contributor" content="F.R. Herrmann" />
<meta name="DC.Contributor" content="P. Giannakopoulos" />
<meta name="article:published_time" content="2017-07-01" />
<meta name="article:section" content="ADULT BRAIN" />
<meta name="citation_title" content="APOE*E4 Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;The presence of &lt;i&gt;apolipoprotein E4&lt;/i&gt; (&lt;i&gt;APOE&lt;/i&gt;*&lt;i&gt;E4&lt;/i&gt;) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of &lt;i&gt;APOE&lt;/i&gt;*&lt;i&gt;E4&lt;/i&gt; on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;This prospective study included 382 community-dwelling elderly controls. At baseline, participants underwent MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel-based morphometry and ROI analysis of GM.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;&lt;i&gt;APOE&lt;/i&gt;*&lt;i&gt;E4&lt;/i&gt;-related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no &lt;i&gt;APOE&lt;/i&gt;*&lt;i&gt;E4-&lt;/i&gt;related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;&lt;i&gt;APOE&lt;/i&gt;*&lt;i&gt;E4&lt;/i&gt;-related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, &lt;i&gt;APOE&lt;/i&gt;*&lt;i&gt;E4&lt;/i&gt; status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.&lt;/p&gt;" />
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<meta name="citation_firstpage" content="1335" />
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<meta name="citation_author" content="S. Haller" />
<meta name="citation_author_institution" content="aFrom the Affidea Centre de Diagnostic Radiologique de Carouge (S.H.), Geneva, Switzerland" />
<meta name="citation_author_institution" content="bFaculty of Medicine (S.H., M.-L.M., F.R.H., P.G.), University of Geneva, Switzerland" />
<meta name="citation_author_institution" content="cDepartments of Surgical Sciences and Radiology (S.H.), Uppsala University, Uppsala, Sweden" />
<meta name="citation_author_institution" content="dDepartment of Neuroradiology (S.H.), University Hospital Freiburg, Freiburg, Germany" />
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<meta name="citation_author" content="M.-L. Montandon" />
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<meta name="twitter:title" content="APOE*E4 Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: The presence of apolipoprotein E4 ( APOE * E4 ) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of APOE * E4 on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.

MATERIALS AND METHODS: This prospective study included 382 community-dwelling elderly controls. At baseline, participants underwent MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel-based morphometry and ROI analysis of GM.

RESULTS: APOE * E4 -related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no APOE * E4- related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.

CONCLUSIONS: APOE * E4 -related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, APOE * E4 status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.

AD
:   Alzheimer disease
APOE 
:   apolipoprotein E 
dCON
:   cognitively deteriorating controls
MCI
:   mild cognitive impairment
sCON
:   cognitively stable controls" />
<meta name="og-title" property="og:title" content="APOE*E4 Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/38/7/1335" />
<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: The presence of apolipoprotein E4 ( APOE * E4 ) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of APOE * E4 on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.

MATERIALS AND METHODS: This prospective study included 382 community-dwelling elderly controls. At baseline, participants underwent MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel-based morphometry and ROI analysis of GM.

RESULTS: APOE * E4 -related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no APOE * E4- related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.

CONCLUSIONS: APOE * E4 -related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, APOE * E4 status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.

AD
:   Alzheimer disease
APOE 
:   apolipoprotein E 
dCON
:   cognitively deteriorating controls
MCI
:   mild cognitive impairment
sCON
:   cognitively stable controls" />
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    <div class="highwire-article-citation highwire-citation-type-highwire-article node55121--5" data-node-nid="55121" id="top-node-55121--6127649720" data-pisa="ajnr;38/7/1335" data-pisa-master="ajnr;ajnr.A5184" data-apath="/ajnr/38/7/1335.atom" data-hw-author-tooltip-instance="highwire_author_tooltip"><div class="highwire-cite highwire-cite-highwire-article highwire-citation-jcore-article-title-complete clearfix has-author-tooltip highwire-citation-highwire-article-top-a">
  
  
      <div class="highwire-cite-overline"><span  class="highwire-cite-metadata-article-type highwire-cite-metadata">Research Article</span><span class="separator-pipe"></span><span  class="highwire-cite-metadata-art-cat highwire-cite-metadata"><span class="wrapper">ADULT BRAIN</span></span></div>
  
      <div class="highwire-cite-access"><span class="highwire-citation-access"><i class="highwire-access-icon highwire-access-icon-open-access open-access hw-icon-open-access" title="Open Access" aria-hidden="true"></i><span  class="element-invisible highwire-access-icon highwire-access-icon-open-access" style="">Open Access</span></span></div>
  
      <h1 class="highwire-cite-title" id="page-title"><em>APOE</em>*<em>E4</em> Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">S. Haller</span>, <span class="highwire-citation-author" data-delta="1">M.-L. Montandon</span>, <span class="highwire-citation-author" data-delta="2">C. Rodriguez</span>, <span class="highwire-citation-author" data-delta="3">M. Ackermann</span>, <span class="highwire-citation-author" data-delta="4">F.R. Herrmann</span> and <span class="highwire-citation-author" data-delta="5">P. Giannakopoulos</span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">July 2017,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">38 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(7) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1335-1342; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A5184 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-55121--6127649720" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">S. Haller </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Affidea Centre de Diagnostic Radiologique de Carouge (S.H.), Geneva, Switzerland</div><div class='author-affiliation'><span class='nlm-sup'>b</span>Faculty of Medicine (S.H., M.-L.M., F.R.H., P.G.), University of Geneva, Switzerland</div><div class='author-affiliation'><span class='nlm-sup'>c</span>Departments of Surgical Sciences and Radiology (S.H.), Uppsala University, Uppsala, Sweden</div><div class='author-affiliation'><span class='nlm-sup'>d</span>Department of Neuroradiology (S.H.), University Hospital Freiburg, Freiburg, Germany</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=S.%2BHaller%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Haller%20S&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AS.%2BHaller%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="http://orcid.org/0000-0001-7433-0203" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for S. Haller</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">M.-L. Montandon </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>b</span>Faculty of Medicine (S.H., M.-L.M., F.R.H., P.G.), University of Geneva, Switzerland</div><div class='author-affiliation'><span class='nlm-sup'>e</span>Department of Mental Health and Psychiatry (M.-L.M., M.A.)</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=M.-L.%2BMontandon%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Montandon%20M&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AM.-L.%2BMontandon%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="http://orcid.org/0000-0002-4983-3201" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for M.-L. Montandon</a></li></ul></div><div class="author-tooltip-2"><div class="author-tooltip-name">C. Rodriguez </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>f</span>Division of Institutional Measures, Medical Direction (C.R., P.G.)</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=C.%2BRodriguez%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Rodriguez%20C&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AC.%2BRodriguez%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="http://orcid.org/0000-0001-6073-2455" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for C. Rodriguez</a></li></ul></div><div class="author-tooltip-3"><div class="author-tooltip-name">M. Ackermann </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>e</span>Department of Mental Health and Psychiatry (M.-L.M., M.A.)</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=M.%2BAckermann%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Ackermann%20M&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AM.%2BAckermann%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="http://orcid.org/0000-0003-3186-5093" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for M. Ackermann</a></li></ul></div><div class="author-tooltip-4"><div class="author-tooltip-name">F.R. Herrmann </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>b</span>Faculty of Medicine (S.H., M.-L.M., F.R.H., P.G.), University of Geneva, Switzerland</div><div class='author-affiliation'><span class='nlm-sup'>g</span>Division of Geriatrics, Department of Internal Medicine, Rehabilitation and Geriatrics (F.R.H.), University Hospitals of Geneva, Geneva, Switzerland.</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=F.R.%2BHerrmann%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Herrmann%20F&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AF.R.%2BHerrmann%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="http://orcid.org/0000-0003-1312-1517" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for F.R. Herrmann</a></li></ul></div><div class="author-tooltip-5"><div class="author-tooltip-name">P. Giannakopoulos </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>b</span>Faculty of Medicine (S.H., M.-L.M., F.R.H., P.G.), University of Geneva, Switzerland</div><div class='author-affiliation'><span class='nlm-sup'>f</span>Division of Institutional Measures, Medical Direction (C.R., P.G.)</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=P.%2BGiannakopoulos%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Giannakopoulos%20P&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AP.%2BGiannakopoulos%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="http://orcid.org/0000-0003-4624-7386" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for P. Giannakopoulos</a></li></ul></div></div></div>  </div>

  
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    <div class="highwire-markup"><div xmlns="http://www.w3.org/1999/xhtml" data-highwire-cite-ref-tooltip-instance="highwire_reflinks_tooltip" class="content-block-markup" xmlns:xhtml="http://www.w3.org/1999/xhtml"><div class="article abstract-view "><span class="highwire-journal-article-marker-start"></span><div class="section abstract" id="abstract-1"><h2>Abstract</h2><div id="sec-1" class="subsection"><p id="p-2"><strong>BACKGROUND AND PURPOSE:</strong> The presence of <em>apolipoprotein E4</em> (<em>APOE</em>*<em>E4</em>) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of <em>APOE</em>*<em>E4</em> on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.</p></div><div id="sec-2" class="subsection"><p id="p-3"><strong>MATERIALS AND METHODS:</strong> This prospective study included 382 community-dwelling elderly controls. At baseline, participants underwent MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel-based morphometry and ROI analysis of GM.</p></div><div id="sec-3" class="subsection"><p id="p-4"><strong>RESULTS:</strong> <em>APOE</em>*<em>E4</em>-related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no <em>APOE</em>*<em>E4-</em>related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.</p></div><div id="sec-4" class="subsection"><p id="p-5"><strong>CONCLUSIONS:</strong> <em>APOE</em>*<em>E4</em>-related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, <em>APOE</em>*<em>E4</em> status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.</p></div></div><div class="section glossary" id="glossary-1"><h2 class="">ABBREVIATIONS:</h2><dl id="def-list-1"><dt id="def-item-1">AD<span class="def-item-dt-sep"></span></dt><dd>Alzheimer disease<span class="def-item-dd-sep"></span></dd><dt id="def-item-2"><em>APOE</em><span class="def-item-dt-sep"></span></dt><dd><em>apolipoprotein E</em><span class="def-item-dd-sep"></span></dd><dt id="def-item-3">dCON<span class="def-item-dt-sep"></span></dt><dd>cognitively deteriorating controls<span class="def-item-dd-sep"></span></dd><dt id="def-item-4">MCI<span class="def-item-dt-sep"></span></dt><dd>mild cognitive impairment<span class="def-item-dd-sep"></span></dd><dt id="def-item-5">sCON<span class="def-item-dt-sep"></span></dt><dd>cognitively stable controls</dd></dl></div><ul class="copyright-statement"><li class="fn" id="copyright-statement-1">© 2017 by American Journal of Neuroradiology</li></ul><div class="license" id="license-1"><p id="p-1">Indicates open access to non-subscribers at <a href="http://www.ajnr.org" rel="license">www.ajnr.org</a></p></div><span class="highwire-journal-article-marker-end"></span></div><span class="related-urls"></span></div><a href="http://ajnr-stage2.stage.highwire.org/content/38/7/1335.full" class="hw-link hw-link-article-full-text" data-icon-position="" data-hide-link-title="0">View Full Text</a></div>  </div>

  
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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 38</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 7 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Jul 2017 </div></div>
      
      
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      <div class="highwire-cite-title"><em>APOE</em>*<em>E4</em> Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline</div>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0"><span class="nlm-given-names">S.</span> <span class="nlm-surname">Haller</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">M.-L.</span> <span class="nlm-surname">Montandon</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">C.</span> <span class="nlm-surname">Rodriguez</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">M.</span> <span class="nlm-surname">Ackermann</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">F.R.</span> <span class="nlm-surname">Herrmann</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">P.</span> <span class="nlm-surname">Giannakopoulos</span></span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-oa-ind highwire-cite-metadata"><i class="highwire-oa-indicator"></i> </span><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">Jul 2017, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">38 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(7) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1335-1342; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A5184 </span></div>
  
  
  
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      <div class="highwire-cite-title"><em>APOE</em>*<em>E4</em> Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline</div>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0"><span class="nlm-given-names">S.</span> <span class="nlm-surname">Haller</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">M.-L.</span> <span class="nlm-surname">Montandon</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">C.</span> <span class="nlm-surname">Rodriguez</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">M.</span> <span class="nlm-surname">Ackermann</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">F.R.</span> <span class="nlm-surname">Herrmann</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">P.</span> <span class="nlm-surname">Giannakopoulos</span></span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-oa-ind highwire-cite-metadata"><i class="highwire-oa-indicator"></i> </span><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">Jul 2017, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">38 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(7) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1335-1342; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A5184 </span></div>
  
  
  
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