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<meta name="DC.Title" content="Dementia, Quantitative Neuroimaging, and Apolipoprotein E Genotype" />
<meta name="DC.Date" content="2000-11-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
<meta name="DC.Rights" content="Copyright © American Society of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Quantitative MR imaging differences in an elderly population of subjects with various clinical disorders (including dementia, particularly Alzheimer's disease and vascular dementia) and disorders of mild cognitive impairment were examined. Potential quantitative MR differences were assessed by presence or absence of the apolipoprotein E ( APOE ) ϵ 4 allele and by level of cognitive deficit.

METHODS: One hundred eighty subjects with a diagnosis of dementia or other clinical disorders were identified from an eligible population of 5677 elderly individuals. Age, duration of disease, and head size (where appropriate) were considered as covariates. APOE genotype was determined by polymerase chain reaction using buccal material. Axial and coronal intermediate- and T2-weighted MR images were quantified using a multispectral segmentation algorithm. Cognitive status was assessed by means of a modified Mini-Mental Status Examination.

RESULTS: All types of dementing illness showed significant volume reductions in the majority of structures examined, particularly in the total brain, hippocampus, and white and gray matter, and increased CSF and ventricular volumes. Subjects with mild cognitive impairment showed fewer atrophic changes but were still distinguishable from the 24 control subjects. Presence of an ϵ 4 allele was associated with smaller hippocampal volume in subjects with Alzheimer's disease and vascular dementia within just 1 year of disease onset. For other analyses, atrophy related to the presence of the ϵ 4 allele disappeared after controlling for age and length of disease.

CONCLUSION: The effects of the ϵ 4 allele on brain morphology may be subtly expressed early in the development of dementia, but do not specifically affect cerebral atrophy thereafter. Cognitive impairment is associated with atrophy irrespective of diagnosis and presence of ϵ 4." />
<meta name="DC.Contributor" content="Erin D. Bigler" />
<meta name="DC.Contributor" content="Christopher M. Lowry" />
<meta name="DC.Contributor" content="Carol V. Anderson" />
<meta name="DC.Contributor" content="Sterling C. Johnson" />
<meta name="DC.Contributor" content="John Terry" />
<meta name="DC.Contributor" content="Marc Steed" />
<meta name="article:published_time" content="2000-11-01" />
<meta name="article:section" content="BRAIN" />
<meta name="citation_title" content="Dementia, Quantitative Neuroimaging, and Apolipoprotein E Genotype" />
<meta name="citation_abstract" lang="en" content="&lt;p&gt;&lt;i&gt;BACKGROUND AND PURPOSE:&lt;/i&gt; Quantitative MR imaging differences in an elderly population of subjects with various clinical disorders (including dementia, particularly Alzheimer9s disease and vascular dementia) and disorders of mild cognitive impairment were examined. Potential quantitative MR differences were assessed by presence or absence of the apolipoprotein E (&lt;i&gt;APOE&lt;/i&gt;) &lt;i&gt;ϵ&lt;/i&gt;4 allele and by level of cognitive deficit.&lt;/p&gt;&lt;p&gt;&lt;i&gt;METHODS:&lt;/i&gt; One hundred eighty subjects with a diagnosis of dementia or other clinical disorders were identified from an eligible population of 5677 elderly individuals. Age, duration of disease, and head size (where appropriate) were considered as covariates. &lt;i&gt;APOE&lt;/i&gt; genotype was determined by polymerase chain reaction using buccal material. Axial and coronal intermediate- and T2-weighted MR images were quantified using a multispectral segmentation algorithm. Cognitive status was assessed by means of a modified Mini-Mental Status Examination.&lt;/p&gt;&lt;p&gt;&lt;i&gt;RESULTS:&lt;/i&gt; All types of dementing illness showed significant volume reductions in the majority of structures examined, particularly in the total brain, hippocampus, and white and gray matter, and increased CSF and ventricular volumes. Subjects with mild cognitive impairment showed fewer atrophic changes but were still distinguishable from the 24 control subjects. Presence of an &lt;i&gt;ϵ&lt;/i&gt;4 allele was associated with smaller hippocampal volume in subjects with Alzheimer9s disease and vascular dementia within just 1 year of disease onset. For other analyses, atrophy related to the presence of the &lt;i&gt;ϵ&lt;/i&gt;4 allele disappeared after controlling for age and length of disease.&lt;/p&gt;&lt;p&gt;&lt;i&gt;CONCLUSION:&lt;/i&gt; The effects of the &lt;i&gt;ϵ&lt;/i&gt;4 allele on brain morphology may be subtly expressed early in the development of dementia, but do not specifically affect cerebral atrophy thereafter. Cognitive impairment is associated with atrophy irrespective of diagnosis and presence of &lt;i&gt;ϵ&lt;/i&gt;4.&lt;/p&gt;" />
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<meta name="twitter:title" content="Dementia, Quantitative Neuroimaging, and Apolipoprotein E Genotype" />
<meta name="twitter:card" content="summary" />
<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Quantitative MR imaging differences in an elderly population of subjects with various clinical disorders (including dementia, particularly Alzheimer's disease and vascular dementia) and disorders of mild cognitive impairment were examined. Potential quantitative MR differences were assessed by presence or absence of the apolipoprotein E ( APOE ) ϵ 4 allele and by level of cognitive deficit.

METHODS: One hundred eighty subjects with a diagnosis of dementia or other clinical disorders were identified from an eligible population of 5677 elderly individuals. Age, duration of disease, and head size (where appropriate) were considered as covariates. APOE genotype was determined by polymerase chain reaction using buccal material. Axial and coronal intermediate- and T2-weighted MR images were quantified using a multispectral segmentation algorithm. Cognitive status was assessed by means of a modified Mini-Mental Status Examination.

RESULTS: All types of dementing illness showed significant volume reductions in the majority of structures examined, particularly in the total brain, hippocampus, and white and gray matter, and increased CSF and ventricular volumes. Subjects with mild cognitive impairment showed fewer atrophic changes but were still distinguishable from the 24 control subjects. Presence of an ϵ 4 allele was associated with smaller hippocampal volume in subjects with Alzheimer's disease and vascular dementia within just 1 year of disease onset. For other analyses, atrophy related to the presence of the ϵ 4 allele disappeared after controlling for age and length of disease.

CONCLUSION: The effects of the ϵ 4 allele on brain morphology may be subtly expressed early in the development of dementia, but do not specifically affect cerebral atrophy thereafter. Cognitive impairment is associated with atrophy irrespective of diagnosis and presence of ϵ 4." />
<meta name="og-title" property="og:title" content="Dementia, Quantitative Neuroimaging, and Apolipoprotein E Genotype" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/21/10/1857" />
<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: Quantitative MR imaging differences in an elderly population of subjects with various clinical disorders (including dementia, particularly Alzheimer's disease and vascular dementia) and disorders of mild cognitive impairment were examined. Potential quantitative MR differences were assessed by presence or absence of the apolipoprotein E ( APOE ) ϵ 4 allele and by level of cognitive deficit.

METHODS: One hundred eighty subjects with a diagnosis of dementia or other clinical disorders were identified from an eligible population of 5677 elderly individuals. Age, duration of disease, and head size (where appropriate) were considered as covariates. APOE genotype was determined by polymerase chain reaction using buccal material. Axial and coronal intermediate- and T2-weighted MR images were quantified using a multispectral segmentation algorithm. Cognitive status was assessed by means of a modified Mini-Mental Status Examination.

RESULTS: All types of dementing illness showed significant volume reductions in the majority of structures examined, particularly in the total brain, hippocampus, and white and gray matter, and increased CSF and ventricular volumes. Subjects with mild cognitive impairment showed fewer atrophic changes but were still distinguishable from the 24 control subjects. Presence of an ϵ 4 allele was associated with smaller hippocampal volume in subjects with Alzheimer's disease and vascular dementia within just 1 year of disease onset. For other analyses, atrophy related to the presence of the ϵ 4 allele disappeared after controlling for age and length of disease.

CONCLUSION: The effects of the ϵ 4 allele on brain morphology may be subtly expressed early in the development of dementia, but do not specifically affect cerebral atrophy thereafter. Cognitive impairment is associated with atrophy irrespective of diagnosis and presence of ϵ 4." />
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      <h1 class="highwire-cite-title" id="page-title">Dementia, Quantitative Neuroimaging, and Apolipoprotein E Genotype</h1>  
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    	<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">November 2000,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">21 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(10) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1857-1868; </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-2459--61840567482" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">Erin D. Bigler </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=Erin%2BD.%2BBigler%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=Bigler%20ED&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%3AErin%2BD.%2BBigler%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">Christopher M. 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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 21</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 10 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Nov 2000 </div></div>
      
      
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