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<meta name="DC.Title" content="Apolipoprotein E ε4 Does Not Modulate Amyloid-β–Associated Neurodegeneration in Preclinical Alzheimer Disease" />
<meta name="DC.Identifier" content="10.3174/ajnr.A3267" />
<meta name="DC.Date" content="2013-03-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Among cognitively healthy older individuals, the relationship among the 2 hallmark proteins of AD (Aβ and τ APOE ε4) and neurodegeneration is not well-understood. Here, we investigated the relationship between Aβ, p-τ, and APOE ε4 on longitudinal brain atrophy in preclinical AD.

MATERIALS AND METHODS: We examined 107 cognitively healthy older adults who underwent longitudinal MR imaging and baseline lumbar puncture. Within the same linear mixed-effects model, we concurrently investigated main and interactive effects between the APOE ε4 genotype and CSF Aβ1–42, CSF p-τ and CSF Aβ1–42, and the APOE ε4 genotype and CSF p-τ on entorhinal cortex atrophy rate. We also examined the relationship of APOE ε4, CSF p-τ, and CSF Aβ1–42 on the atrophy rate of other AD-vulnerable neuroanatomic regions.

RESULTS: The full model with main and interactive effects demonstrated a significant interaction only between CSF p-τ and CSF Aβ1–42 on entorhinal cortex atrophy rate, indicating elevated atrophy with time in individuals with increased CSF p-τ and decreased CSF Aβ1–42. The APOE ε4 genotype was significantly and specifically associated with CSF Aβ1–42. However, the interaction between the APOE ε4 genotype and either CSF Aβ1–42 or CSF p-τ on entorhinal cortex atrophy rate was not significant. We found similar results in other AD-vulnerable regions.

CONCLUSIONS: On the basis of our findings and building on prior experimental evidence, we propose a model of the pathogenic cascade underlying preclinical AD in which APOE ε4 primarily influences the pathology of Alzheimer disease via Aβ-related mechanisms, and in turn, Aβ-associated neurodegeneration occurs only in the presence of p-τ.

Aβ
:   amyloid-β
AD
:   Alzheimer disease
APOE ε4
:   ε4 allele of apolipoprotein E 
HC
:   healthy controls
p-τ
:   phospho-τ181p
SE
:   standard error of the mean" />
<meta name="DC.Contributor" content="R.S. Desikan" />
<meta name="DC.Contributor" content="L.K. McEvoy" />
<meta name="DC.Contributor" content="D. Holland" />
<meta name="DC.Contributor" content="W.K. Thompson" />
<meta name="DC.Contributor" content="J.B. Brewer" />
<meta name="DC.Contributor" content="P.S. Aisen" />
<meta name="DC.Contributor" content="O.A. Andreassen" />
<meta name="DC.Contributor" content="B.T. Hyman" />
<meta name="DC.Contributor" content="R.A. Sperling" />
<meta name="DC.Contributor" content="A.M. Dale" />
<meta name="DC.Contributor" content="for the Alzheimer's Disease Neuroimaging Initiative" />
<meta name="article:published_time" content="2013-03-01" />
<meta name="article:section" content="Brain" />
<meta name="citation_title" content="Apolipoprotein E ε4 Does Not Modulate Amyloid-β–Associated Neurodegeneration in Preclinical Alzheimer Disease" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;Among cognitively healthy older individuals, the relationship among the 2 hallmark proteins of AD (Aβ and τ &lt;i&gt;APOE&lt;/i&gt; ε4) and neurodegeneration is not well-understood. Here, we investigated the relationship between Aβ, p-τ, and &lt;i&gt;APOE&lt;/i&gt; ε4 on longitudinal brain atrophy in preclinical AD.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;We examined 107 cognitively healthy older adults who underwent longitudinal MR imaging and baseline lumbar puncture. Within the same linear mixed-effects model, we concurrently investigated main and interactive effects between the &lt;i&gt;APOE&lt;/i&gt; ε4 genotype and CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt;, CSF p-τ and CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt;, and the &lt;i&gt;APOE&lt;/i&gt; ε4 genotype and CSF p-τ on entorhinal cortex atrophy rate. We also examined the relationship of &lt;i&gt;APOE&lt;/i&gt; ε4, CSF p-τ, and CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt; on the atrophy rate of other AD-vulnerable neuroanatomic regions.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;The full model with main and interactive effects demonstrated a significant interaction only between CSF p-τ and CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt; on entorhinal cortex atrophy rate, indicating elevated atrophy with time in individuals with increased CSF p-τ and decreased CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt;. The &lt;i&gt;APOE&lt;/i&gt; ε4 genotype was significantly and specifically associated with CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt;. However, the interaction between the &lt;i&gt;APOE&lt;/i&gt; ε4 genotype and either CSF Aβ&lt;sub&gt;1–42&lt;/sub&gt; or CSF p-τ on entorhinal cortex atrophy rate was not significant. We found similar results in other AD-vulnerable regions.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;On the basis of our findings and building on prior experimental evidence, we propose a model of the pathogenic cascade underlying preclinical AD in which &lt;i&gt;APOE&lt;/i&gt; ε4 primarily influences the pathology of Alzheimer disease via Aβ-related mechanisms, and in turn, Aβ-associated neurodegeneration occurs only in the presence of p-τ.&lt;/p&gt;" />
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<meta name="twitter:title" content="Apolipoprotein E ε4 Does Not Modulate Amyloid-β–Associated Neurodegeneration in Preclinical Alzheimer Disease" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Among cognitively healthy older individuals, the relationship among the 2 hallmark proteins of AD (Aβ and τ APOE ε4) and neurodegeneration is not well-understood. Here, we investigated the relationship between Aβ, p-τ, and APOE ε4 on longitudinal brain atrophy in preclinical AD.

MATERIALS AND METHODS: We examined 107 cognitively healthy older adults who underwent longitudinal MR imaging and baseline lumbar puncture. Within the same linear mixed-effects model, we concurrently investigated main and interactive effects between the APOE ε4 genotype and CSF Aβ1–42, CSF p-τ and CSF Aβ1–42, and the APOE ε4 genotype and CSF p-τ on entorhinal cortex atrophy rate. We also examined the relationship of APOE ε4, CSF p-τ, and CSF Aβ1–42 on the atrophy rate of other AD-vulnerable neuroanatomic regions.

RESULTS: The full model with main and interactive effects demonstrated a significant interaction only between CSF p-τ and CSF Aβ1–42 on entorhinal cortex atrophy rate, indicating elevated atrophy with time in individuals with increased CSF p-τ and decreased CSF Aβ1–42. The APOE ε4 genotype was significantly and specifically associated with CSF Aβ1–42. However, the interaction between the APOE ε4 genotype and either CSF Aβ1–42 or CSF p-τ on entorhinal cortex atrophy rate was not significant. We found similar results in other AD-vulnerable regions.

CONCLUSIONS: On the basis of our findings and building on prior experimental evidence, we propose a model of the pathogenic cascade underlying preclinical AD in which APOE ε4 primarily influences the pathology of Alzheimer disease via Aβ-related mechanisms, and in turn, Aβ-associated neurodegeneration occurs only in the presence of p-τ.

Aβ
:   amyloid-β
AD
:   Alzheimer disease
APOE ε4
:   ε4 allele of apolipoprotein E 
HC
:   healthy controls
p-τ
:   phospho-τ181p
SE
:   standard error of the mean" />
<meta name="og-title" property="og:title" content="Apolipoprotein E ε4 Does Not Modulate Amyloid-β–Associated Neurodegeneration in Preclinical Alzheimer Disease" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/34/3/505" />
<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: Among cognitively healthy older individuals, the relationship among the 2 hallmark proteins of AD (Aβ and τ APOE ε4) and neurodegeneration is not well-understood. Here, we investigated the relationship between Aβ, p-τ, and APOE ε4 on longitudinal brain atrophy in preclinical AD.

MATERIALS AND METHODS: We examined 107 cognitively healthy older adults who underwent longitudinal MR imaging and baseline lumbar puncture. Within the same linear mixed-effects model, we concurrently investigated main and interactive effects between the APOE ε4 genotype and CSF Aβ1–42, CSF p-τ and CSF Aβ1–42, and the APOE ε4 genotype and CSF p-τ on entorhinal cortex atrophy rate. We also examined the relationship of APOE ε4, CSF p-τ, and CSF Aβ1–42 on the atrophy rate of other AD-vulnerable neuroanatomic regions.

RESULTS: The full model with main and interactive effects demonstrated a significant interaction only between CSF p-τ and CSF Aβ1–42 on entorhinal cortex atrophy rate, indicating elevated atrophy with time in individuals with increased CSF p-τ and decreased CSF Aβ1–42. The APOE ε4 genotype was significantly and specifically associated with CSF Aβ1–42. However, the interaction between the APOE ε4 genotype and either CSF Aβ1–42 or CSF p-τ on entorhinal cortex atrophy rate was not significant. We found similar results in other AD-vulnerable regions.

CONCLUSIONS: On the basis of our findings and building on prior experimental evidence, we propose a model of the pathogenic cascade underlying preclinical AD in which APOE ε4 primarily influences the pathology of Alzheimer disease via Aβ-related mechanisms, and in turn, Aβ-associated neurodegeneration occurs only in the presence of p-τ.

Aβ
:   amyloid-β
AD
:   Alzheimer disease
APOE ε4
:   ε4 allele of apolipoprotein E 
HC
:   healthy controls
p-τ
:   phospho-τ181p
SE
:   standard error of the mean" />
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    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">R.S. Desikan</span>, <span class="highwire-citation-author" data-delta="1">L.K. McEvoy</span>, <span class="highwire-citation-author" data-delta="2">D. Holland</span>, <span class="highwire-citation-author" data-delta="3">W.K. Thompson</span>, <span class="highwire-citation-author" data-delta="4">J.B. Brewer</span>, <span class="highwire-citation-author" data-delta="5">P.S. Aisen</span>, <span class="highwire-citation-author" data-delta="6">O.A. Andreassen</span>, <span class="highwire-citation-author" data-delta="7">B.T. Hyman</span>, <span class="highwire-citation-author" data-delta="8">R.A. Sperling</span>, <span class="highwire-citation-author" data-delta="9">A.M. Dale</span> and <span class="highwire-citation-author" data-delta="10"><span class="nlm-collab" data-xlink-type="simple" data-hwp-id="collab-1">for the Alzheimer's Disease Neuroimaging Initiative</span></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">March 2013,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">34 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(3) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">505-510; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A3267 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-12294--8870399541" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">R.S. Desikan </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Departments of Radiology (R.S.D., L.K.E., J.B.B., A.M.D.)</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=R.S.%2BDesikan%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=Desikan%20R&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 last"><a href="/search/author1%3AR.S.%2BDesikan%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">L.K. 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    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">vol. 34 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">no. 3 </span><span  class="highwire-cite-metadata-page-string highwire-cite-metadata">505-510 </span></div>
  
  
  
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    <div class="highwire-markup"><div xmlns="http://www.w3.org/1999/xhtml" class="content-block-markup" xmlns:xhtml="http://www.w3.org/1999/xhtml"><div xmlns:xhtml="http://www.w3.org/1999/xhtml" class="contributors"><ol class="contributor-list" id="contrib-group-1"><li class="contributor" id="contrib-1"><span class="name">R.S. Desikan</span><a id="xref-aff-1-1" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-2"><span class="name">L.K. McEvoy</span><a id="xref-aff-1-2" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-3"><span class="name">D. Holland</span><a id="xref-aff-2-1" class="xref-aff" href="#aff-2">b</a>, </li><li class="contributor" id="contrib-4"><span class="name">W.K. Thompson</span><a id="xref-aff-3-1" class="xref-aff" href="#aff-3">c</a>, </li><li class="contributor" id="contrib-5"><span class="name">J.B. Brewer</span><a id="xref-aff-1-3" class="xref-aff" href="#aff-1">a</a><span class="xref-sep">,</span><a id="xref-aff-2-2" class="xref-aff" href="#aff-2">b</a>, </li><li class="contributor" id="contrib-6"><span class="name">P.S. Aisen</span><a id="xref-aff-2-3" class="xref-aff" href="#aff-2">b</a>, </li><li class="contributor" id="contrib-7"><span class="name">O.A. Andreassen</span><a id="xref-aff-3-2" class="xref-aff" href="#aff-3">c</a><span class="xref-sep">,</span><a id="xref-aff-4-1" class="xref-aff" href="#aff-4">d</a>, </li><li class="contributor" id="contrib-8"><span class="name">B.T. Hyman</span><a id="xref-aff-5-1" class="xref-aff" href="#aff-5">e</a>, </li><li class="contributor" id="contrib-9"><span class="name">R.A. Sperling</span><a id="xref-aff-5-2" class="xref-aff" href="#aff-5">e</a><span class="xref-sep">,</span><a id="xref-aff-6-1" class="xref-aff" href="#aff-6">f</a>, </li><li class="contributor" id="contrib-10"><span class="name">A.M. Dale</span><a id="xref-aff-1-4" class="xref-aff" href="#aff-1">a</a><span class="xref-sep">,</span><a id="xref-aff-2-4" class="xref-aff" href="#aff-2">b</a>, </li><li class="last" id="contrib-11"><span class="collab" id="collab-1">for the Alzheimer's Disease Neuroimaging Initiative</span></li></ol><ol class="affiliation-list"><li class="aff"><a id="aff-1" name="aff-1"></a><address><sup>a</sup>From the Departments of Radiology (R.S.D., L.K.E., J.B.B., A.M.D.)</address></li><li class="aff"><a id="aff-2" name="aff-2"></a><address><sup>b</sup>Neuroscience (D.H., J.B.B., P.S.A., A.M.D.)</address></li><li class="aff"><a id="aff-3" name="aff-3"></a><address><sup>c</sup>Psychiatry (W.K.T., O.A.A.), University of California, San Diego, La Jolla, California</address></li><li class="aff"><a id="aff-4" name="aff-4"></a><address><sup>d</sup>Institute of Clinical Medicine (O.A.A.), University of Oslo and Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway</address></li><li class="aff"><a id="aff-5" name="aff-5"></a><address><sup>e</sup>Department of Neurology (B.T.H., R.A.S.), Massachusetts General Hospital, Boston, Massachusetts</address></li><li class="aff"><a id="aff-6" name="aff-6"></a><address><sup>f</sup>Department of Neurology (R.A.S.), Brigham and Women's Hospital, Boston, Massachusetts.</address></li></ol><ol class="corresp-list"><li class="corresp" id="corresp-1">Please address correspondence to Rahul S. Desikan, MD, PhD, <span class="addr-line">Department of Radiology, University of California, San Diego, 8950 Villa La Jolla Dr, Suite C101, La Jolla, California 92037-0841</span>; e-mail: <span class="em-link"><span class="em-addr">rdesikan{at}ucsd.edu</span></span></li></ol></div></div><a href="http://ajnr-stage2.stage.highwire.org/content/34/3/505.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-title"><em>Apolipoprotein E</em> ε4 Does Not Modulate Amyloid-β–Associated Neurodegeneration in Preclinical Alzheimer Disease</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">R.S.</span> <span class="nlm-surname">Desikan</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">L.K.</span> <span class="nlm-surname">McEvoy</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">D.</span> <span class="nlm-surname">Holland</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">W.K.</span> <span class="nlm-surname">Thompson</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">J.B.</span> <span class="nlm-surname">Brewer</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">P.S.</span> <span class="nlm-surname">Aisen</span></span>, <span class="highwire-citation-author" data-delta="6"><span class="nlm-given-names">O.A.</span> <span class="nlm-surname">Andreassen</span></span>, <span class="highwire-citation-author" data-delta="7"><span class="nlm-given-names">B.T.</span> <span class="nlm-surname">Hyman</span></span>, <span class="highwire-citation-author" data-delta="8"><span class="nlm-given-names">R.A.</span> <span class="nlm-surname">Sperling</span></span>, <span class="highwire-citation-author" data-delta="9"><span class="nlm-given-names">A.M.</span> <span class="nlm-surname">Dale</span></span>, <span class="highwire-citation-author" data-delta="10"><span class="nlm-collab" data-xlink-type="simple" data-hwp-id="collab-1">for the Alzheimer's Disease Neuroimaging Initiative</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">Mar 2013, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">34 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(3) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">505-510; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A3267 </span></div>
  
  
  
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      <div class="highwire-cite-title"><em>Apolipoprotein E</em> ε4 Does Not Modulate Amyloid-β–Associated Neurodegeneration in Preclinical Alzheimer Disease</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">R.S.</span> <span class="nlm-surname">Desikan</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">L.K.</span> <span class="nlm-surname">McEvoy</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">D.</span> <span class="nlm-surname">Holland</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">W.K.</span> <span class="nlm-surname">Thompson</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">J.B.</span> <span class="nlm-surname">Brewer</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">P.S.</span> <span class="nlm-surname">Aisen</span></span>, <span class="highwire-citation-author" data-delta="6"><span class="nlm-given-names">O.A.</span> <span class="nlm-surname">Andreassen</span></span>, <span class="highwire-citation-author" data-delta="7"><span class="nlm-given-names">B.T.</span> <span class="nlm-surname">Hyman</span></span>, <span class="highwire-citation-author" data-delta="8"><span class="nlm-given-names">R.A.</span> <span class="nlm-surname">Sperling</span></span>, <span class="highwire-citation-author" data-delta="9"><span class="nlm-given-names">A.M.</span> <span class="nlm-surname">Dale</span></span>, <span class="highwire-citation-author" data-delta="10"><span class="nlm-collab" data-xlink-type="simple" data-hwp-id="collab-1">for the Alzheimer's Disease Neuroimaging Initiative</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">Mar 2013, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">34 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(3) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">505-510; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A3267 </span></div>
  
  
  
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