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<meta name="DC.Title" content="Regional Neuronal Network Failure and Cognition in Late-Onset Sporadic Alzheimer Disease" />
<meta name="DC.Identifier" content="10.3174/ajnr.A3895" />
<meta name="DC.Date" content="2014-06-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: The severe cognitive deficits in Alzheimer disease are associated with structural lesions in gray and white matter in addition to changes in synaptic function. The current investigation studied the breakdown of the structure and function in regional networks involving the Papez circuit and extended neocortical association areas.

MATERIALS AND METHODS: Cortical volumetric and diffusion tensor imaging (3T MR imaging), positron-emission tomography with 18F fluorodeoxyglucose on a high-resolution research tomograph, and comprehensive neuropsychological assessments were performed in patients with late-onset sporadic Alzheimer disease, those with mild cognitive impairment, and elderly healthy controls.

RESULTS: Atrophy of the medial temporal lobes was the strongest and most consistent abnormality in patients with mild cognitive impairment and Alzheimer disease. Atrophy in the temporal, frontal, and parietal regions was most strongly related to episodic memory deficits, while deficits in semantic cognition were also strongly related to reductions of glucose metabolism in the posterior cingulate cortex and temporoparietal regions. Changes in fractional anisotropy within white matter tracts, particularly in the left cingulum bundle, uncinate fasciculus, superior longitudinal fasciculus, and inferior fronto-occipital fasciculus, were significantly associated with the cognitive deficits in multiple regression analyses. Posterior cingulate and orbitofrontal metabolic deficits appeared to be related to microstructural changes in projecting white matter tracts.

CONCLUSIONS: Many lesioned network components within the Papez circuit and extended neocortical association areas were significantly associated with cognitive dysfunction in both mild cognitive impairment and late-onset sporadic Alzheimer disease. Hippocampal atrophy was the most prominent lesion, with associated impairment of the uncinate and cingulum white matter microstructures and hippocampal and posterior cingulate metabolic impairment.

ACE-R
:   Addenbrooke's Cognitive Examination-Revised
AD
:   Alzheimer disease
FA
:   fractional anisotropy
HCMP
:   hippocampus
MCI
:   mild cognitive impairment
MTL
:   medial temporal lobe
PCC
:   posterior cingulate cortex
TBSS
:   Tract-Based Spatial Statistics" />
<meta name="DC.Contributor" content="S.F. Carter" />
<meta name="DC.Contributor" content="K.V. Embleton" />
<meta name="DC.Contributor" content="J.M. Anton-Rodriguez" />
<meta name="DC.Contributor" content="A. Burns" />
<meta name="DC.Contributor" content="M.A.L. Ralph" />
<meta name="DC.Contributor" content="K. Herholz" />
<meta name="article:published_time" content="2014-06-01" />
<meta name="article:section" content="Original Research" />
<meta name="citation_title" content="Regional Neuronal Network Failure and Cognition in Late-Onset Sporadic Alzheimer Disease" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;The severe cognitive deficits in Alzheimer disease are associated with structural lesions in gray and white matter in addition to changes in synaptic function. The current investigation studied the breakdown of the structure and function in regional networks involving the Papez circuit and extended neocortical association areas.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;Cortical volumetric and diffusion tensor imaging (3T MR imaging), positron-emission tomography with &lt;sup&gt;18&lt;/sup&gt;F fluorodeoxyglucose on a high-resolution research tomograph, and comprehensive neuropsychological assessments were performed in patients with late-onset sporadic Alzheimer disease, those with mild cognitive impairment, and elderly healthy controls.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;Atrophy of the medial temporal lobes was the strongest and most consistent abnormality in patients with mild cognitive impairment and Alzheimer disease. Atrophy in the temporal, frontal, and parietal regions was most strongly related to episodic memory deficits, while deficits in semantic cognition were also strongly related to reductions of glucose metabolism in the posterior cingulate cortex and temporoparietal regions. Changes in fractional anisotropy within white matter tracts, particularly in the left cingulum bundle, uncinate fasciculus, superior longitudinal fasciculus, and inferior fronto-occipital fasciculus, were significantly associated with the cognitive deficits in multiple regression analyses. Posterior cingulate and orbitofrontal metabolic deficits appeared to be related to microstructural changes in projecting white matter tracts.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;Many lesioned network components within the Papez circuit and extended neocortical association areas were significantly associated with cognitive dysfunction in both mild cognitive impairment and late-onset sporadic Alzheimer disease. Hippocampal atrophy was the most prominent lesion, with associated impairment of the uncinate and cingulum white matter microstructures and hippocampal and posterior cingulate metabolic impairment.&lt;/p&gt;" />
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<meta name="twitter:title" content="Regional Neuronal Network Failure and Cognition in Late-Onset Sporadic Alzheimer Disease" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: The severe cognitive deficits in Alzheimer disease are associated with structural lesions in gray and white matter in addition to changes in synaptic function. The current investigation studied the breakdown of the structure and function in regional networks involving the Papez circuit and extended neocortical association areas.

MATERIALS AND METHODS: Cortical volumetric and diffusion tensor imaging (3T MR imaging), positron-emission tomography with 18F fluorodeoxyglucose on a high-resolution research tomograph, and comprehensive neuropsychological assessments were performed in patients with late-onset sporadic Alzheimer disease, those with mild cognitive impairment, and elderly healthy controls.

RESULTS: Atrophy of the medial temporal lobes was the strongest and most consistent abnormality in patients with mild cognitive impairment and Alzheimer disease. Atrophy in the temporal, frontal, and parietal regions was most strongly related to episodic memory deficits, while deficits in semantic cognition were also strongly related to reductions of glucose metabolism in the posterior cingulate cortex and temporoparietal regions. Changes in fractional anisotropy within white matter tracts, particularly in the left cingulum bundle, uncinate fasciculus, superior longitudinal fasciculus, and inferior fronto-occipital fasciculus, were significantly associated with the cognitive deficits in multiple regression analyses. Posterior cingulate and orbitofrontal metabolic deficits appeared to be related to microstructural changes in projecting white matter tracts.

CONCLUSIONS: Many lesioned network components within the Papez circuit and extended neocortical association areas were significantly associated with cognitive dysfunction in both mild cognitive impairment and late-onset sporadic Alzheimer disease. Hippocampal atrophy was the most prominent lesion, with associated impairment of the uncinate and cingulum white matter microstructures and hippocampal and posterior cingulate metabolic impairment.

ACE-R
:   Addenbrooke's Cognitive Examination-Revised
AD
:   Alzheimer disease
FA
:   fractional anisotropy
HCMP
:   hippocampus
MCI
:   mild cognitive impairment
MTL
:   medial temporal lobe
PCC
:   posterior cingulate cortex
TBSS
:   Tract-Based Spatial Statistics" />
<meta name="og-title" property="og:title" content="Regional Neuronal Network Failure and Cognition in Late-Onset Sporadic Alzheimer Disease" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/35/6_suppl/S18" />
<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 severe cognitive deficits in Alzheimer disease are associated with structural lesions in gray and white matter in addition to changes in synaptic function. The current investigation studied the breakdown of the structure and function in regional networks involving the Papez circuit and extended neocortical association areas.

MATERIALS AND METHODS: Cortical volumetric and diffusion tensor imaging (3T MR imaging), positron-emission tomography with 18F fluorodeoxyglucose on a high-resolution research tomograph, and comprehensive neuropsychological assessments were performed in patients with late-onset sporadic Alzheimer disease, those with mild cognitive impairment, and elderly healthy controls.

RESULTS: Atrophy of the medial temporal lobes was the strongest and most consistent abnormality in patients with mild cognitive impairment and Alzheimer disease. Atrophy in the temporal, frontal, and parietal regions was most strongly related to episodic memory deficits, while deficits in semantic cognition were also strongly related to reductions of glucose metabolism in the posterior cingulate cortex and temporoparietal regions. Changes in fractional anisotropy within white matter tracts, particularly in the left cingulum bundle, uncinate fasciculus, superior longitudinal fasciculus, and inferior fronto-occipital fasciculus, were significantly associated with the cognitive deficits in multiple regression analyses. Posterior cingulate and orbitofrontal metabolic deficits appeared to be related to microstructural changes in projecting white matter tracts.

CONCLUSIONS: Many lesioned network components within the Papez circuit and extended neocortical association areas were significantly associated with cognitive dysfunction in both mild cognitive impairment and late-onset sporadic Alzheimer disease. Hippocampal atrophy was the most prominent lesion, with associated impairment of the uncinate and cingulum white matter microstructures and hippocampal and posterior cingulate metabolic impairment.

ACE-R
:   Addenbrooke's Cognitive Examination-Revised
AD
:   Alzheimer disease
FA
:   fractional anisotropy
HCMP
:   hippocampus
MCI
:   mild cognitive impairment
MTL
:   medial temporal lobe
PCC
:   posterior cingulate cortex
TBSS
:   Tract-Based Spatial Statistics" />
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    <title>Regional Neuronal Network Failure and Cognition in Late-Onset Sporadic Alzheimer Disease | American Journal of Neuroradiology</title>  
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    <div class="highwire-article-citation highwire-citation-type-highwire-article node13726--5" data-node-nid="13726" id="top-node-13726--679202914" data-pisa="ajnr;35/6_suppl/S18" data-pisa-master="ajnr;ajnr.A3895" data-apath="/ajnr/35/6_suppl/S18.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">Original Research</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">Regional Neuronal Network Failure and Cognition in Late-Onset Sporadic Alzheimer Disease</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">S.F. Carter</span>, <span class="highwire-citation-author" data-delta="1">K.V. Embleton</span>, <span class="highwire-citation-author" data-delta="2">J.M. Anton-Rodriguez</span>, <span class="highwire-citation-author" data-delta="3">A. Burns</span>, <span class="highwire-citation-author" data-delta="4">M.A.L. Ralph</span> and <span class="highwire-citation-author" data-delta="5">K. Herholz</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">June 2014,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">35 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(6 suppl) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">S18-S30; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A3895 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-13726--679202914" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">S.F. Carter </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Wolfson Molecular Imaging Centre (S.F.C., J.M.A.-R., K.H.)</div><div class='author-affiliation'><span class='nlm-sup'>b</span>Institute of Population Health, Neuroscience and Aphasia Research Unit (S.F.C., M.A.L.R.)</div><div class='author-affiliation'><span class='nlm-sup'>e</span>Alzheimer Neurobiology Centre (S.F.C.), Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.</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.F.%2BCarter%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=Carter%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 last"><a href="/search/author1%3AS.F.%2BCarter%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">K.V. Embleton </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>c</span>School of Psychological Sciences (K.V.E.)</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=K.V.%2BEmbleton%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=Embleton%20K&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%3AK.V.%2BEmbleton%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-2"><div class="author-tooltip-name">J.M. Anton-Rodriguez </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Wolfson Molecular Imaging Centre (S.F.C., J.M.A.-R., K.H.)</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=J.M.%2BAnton-Rodriguez%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=Anton-Rodriguez%20J&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%3AJ.M.%2BAnton-Rodriguez%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-3"><div class="author-tooltip-name">A. Burns </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>d</span>Institute of Brain, Behaviour and Mental Health (A.B., K.H.), University of Manchester, Manchester, UK</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=A.%2BBurns%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=Burns%20A&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%3AA.%2BBurns%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-4"><div class="author-tooltip-name">M.A.L. Ralph </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>b</span>Institute of Population Health, Neuroscience and Aphasia Research Unit (S.F.C., M.A.L.R.)</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.A.L.%2BRalph%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=Ralph%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 last"><a href="/search/author1%3AM.A.L.%2BRalph%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-5"><div class="author-tooltip-name">K. Herholz </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Wolfson Molecular Imaging Centre (S.F.C., J.M.A.-R., K.H.)</div><div class='author-affiliation'><span class='nlm-sup'>d</span>Institute of Brain, Behaviour and Mental Health (A.B., K.H.), University of Manchester, Manchester, UK</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=K.%2BHerholz%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=Herholz%20K&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%3AK.%2BHerholz%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div></div></div>  </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">S.F. Carter</span><a id="xref-aff-1-1" class="xref-aff" href="#aff-1">a</a><span class="xref-sep">,</span><a id="xref-aff-2-1" class="xref-aff" href="#aff-2">b</a><span class="xref-sep">,</span><a id="xref-aff-5-1" class="xref-aff" href="#aff-5">e</a>, </li><li class="contributor" id="contrib-2"><span class="name">K.V. Embleton</span><a id="xref-aff-3-1" class="xref-aff" href="#aff-3">c</a>, </li><li class="contributor" id="contrib-3"><span class="name">J.M. Anton-Rodriguez</span><a id="xref-aff-1-2" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-4"><span class="name">A. Burns</span><a id="xref-aff-4-1" class="xref-aff" href="#aff-4">d</a>, </li><li class="contributor" id="contrib-5"><span class="name">M.A.L. Ralph</span><a id="xref-aff-2-2" class="xref-aff" href="#aff-2">b</a> and </li><li class="last" id="contrib-6"><span class="name">K. Herholz</span><a id="xref-aff-1-3" class="xref-aff" href="#aff-1">a</a><span class="xref-sep">,</span><a id="xref-aff-4-2" class="xref-aff" href="#aff-4">d</a></li></ol><ol class="affiliation-list"><li class="aff"><a id="aff-1" name="aff-1"></a><address><sup>a</sup>From the Wolfson Molecular Imaging Centre (S.F.C., J.M.A.-R., K.H.)</address></li><li class="aff"><a id="aff-2" name="aff-2"></a><address><sup>b</sup>Institute of Population Health, Neuroscience and Aphasia Research Unit (S.F.C., M.A.L.R.)</address></li><li class="aff"><a id="aff-3" name="aff-3"></a><address><sup>c</sup>School of Psychological Sciences (K.V.E.)</address></li><li class="aff"><a id="aff-4" name="aff-4"></a><address><sup>d</sup>Institute of Brain, Behaviour and Mental Health (A.B., K.H.), University of Manchester, Manchester, UK</address></li><li class="aff"><a id="aff-5" name="aff-5"></a><address><sup>e</sup>Alzheimer Neurobiology Centre (S.F.C.), Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.</address></li></ol><ol class="corresp-list"><li class="corresp" id="corresp-1">Please address correspondence to Prof. Karl Herholz, MD, <span class="addr-line">Wolfson Molecular Imaging Centre, University of Manchester, 27 Palatine Rd, Withington, Manchester, M20 3LJ, UK</span>; e-mail: <span class="em-link"><span class="em-addr">karl.herholz{at}manchester.ac.uk</span></span></li></ol></div></div><a href="http://ajnr-stage2.stage.highwire.org/content/35/6_suppl/S18.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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