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<front>
<journal-meta>
<journal-id journal-id-type="issn">1043-3155</journal-id>
<journal-id journal-id-type="nlm-ta">Pediatr Neurol Briefs</journal-id>
<journal-id journal-id-type="pmc">pedneurbriefs</journal-id>
<journal-id journal-id-type="iso-abbrev">Pediatr Neurol Briefs</journal-id>
<journal-title-group>
<journal-title>Pediatric Neurology Briefs</journal-title>
<abbrev-journal-title>Pediatr Neurol Briefs</abbrev-journal-title>
</journal-title-group>
<issn pub-type="epub">2166-6482</issn>
<issn pub-type="ppub">1043-3155</issn>
<issn-l>2166-3155</issn-l>
<publisher>
<publisher-name>Pediatric Neurology Briefs Publishers</publisher-name>
<publisher-loc>Chicago, IL, USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="publisher-id">PNB-2014-28-3-7</article-id>
<article-id pub-id-type="doi">10.15844/pedneurbriefs-28-3-7</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Degenerative Diseases</subject>
</subj-group>
<subj-group subj-group-type="Discipline-v2">
<subject>Neurology</subject>
<subject>Pediatrics</subject>
<subject>Nervous System Diseases</subject>
<subject>Child Development</subject>
<subject>Brain Diseases</subject>
<subject>Neurosurgery</subject>
<subject>Child</subject>
<subject>Infant</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Alzheimer Gene Linked to Brain Development</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<contrib-id contrib-id-type="orcid">http://orcid.org/0000-0002-0173-7931</contrib-id>
<name>
<surname>Millichap</surname>
<given-names>J. Gordon</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="AF0001">1</xref>
<xref ref-type="aff" rid="AF0002">2</xref>
<xref ref-type="corresp" rid="cor1">&#x002A;</xref>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">http://orcid.org/0000-0002-0798-0131</contrib-id>
<name>
<surname>Millichap</surname>
<given-names>John J.</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="AF0001">1</xref>
<xref ref-type="aff" rid="AF0002">2</xref>
</contrib>
</contrib-group>
<aff id="AF0001">
<label>1</label>Division of Neurology, Ann &#x0026; Robert H. Lurie Children&#x0027;s Hospital of Chicago, Chicago, IL</aff>
<aff id="AF0002">
<label>2</label>Departments of Pediatrics and Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL</aff>
<author-notes>
<corresp id="cor1">
<label>&#x002A;</label>Correspondence: Dr. J. Gordon Millichap, E-mail: <email xlink:href="jgmillichap@northwestern.edu">jgmillichap@northwestern.edu</email>
</corresp>
</author-notes>
<pub-date date-type="pub" publication-format="print">
<month>03</month>
<year>2014</year>
</pub-date>
<pub-date date-type="pub" publication-format="electronic">
<day>31</day>
<month>10</month>
<year>2015</year>
</pub-date>
<volume>28</volume>
<issue>3</issue>
<fpage>22</fpage>
<lpage>23</lpage>
<permissions>
<copyright-statement>Copyright: &#x00A9; 2014 The Author(s)</copyright-statement>
<copyright-year>2014</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/">
<license-p>This work is licensed under the <uri xlink:href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution 4.0 International License</uri>, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<related-article id="R1" related-article-type="commentary-article" ext-link-type="doi" xlink:href="10.1001/jamaneurol.2013.4544" vol="71" page="11">
<article-title>Brain differences in infants at differential genetic risk for late-onset Alzheimer disease: a cross-sectional imaging study</article-title>
</related-article>
<abstract abstract-type="web-summary" specific-use="electronic-only">
<p>Investigators at Brown University, Providence, RI, and other imaging genetic centers in the US, compare MRI measurements of white matter myelin water fraction (MWF) and gray matter volume (GMV) in healthy infant carriers and noncarriers of the apolipoprotein E (APOE) e4 allele, the major susceptibility gene for late-onset Alzheimer disease (AD).</p>
</abstract>
<kwd-group>
<kwd>Myelin Water Fraction</kwd>
<kwd>Gray Matter Volume</kwd>
<kwd>Alzheimer Disease</kwd>
</kwd-group>
</article-meta>
</front>
<body>
<p>Investigators at Brown University, Providence, RI, and other imaging genetic centers in the US, compare MRI measurements of white matter myelin water fraction (MWF) and gray matter volume (GMV) in healthy infant carriers and noncarriers of the apolipoprotein E (APOE) e4 allele, the major susceptibility gene for late-onset Alzheimer disease (AD). Infant e4 carriers, ages 2&#x2013;25 months, had lower MWF and GMV measurements than noncarriers in precuneus, posterior/middle cingulate, lateral temporal, and medial occipitotemporal regions, areas affected by AD, whereas these measures were greater in frontal regions, and an attenuated relationship between MWF and age was evident in posterior white matter regions. The study demonstrates some of the earliest brain changes associated with a genetic predisposition to AD, and the role of APOE in normal human brain development and AD pathology. [<xref ref-type="bibr" rid="CIT0001">1</xref>]</p>
<p>COMMENTARY. In a comment (Alzheimer gene APOE e4 linked to brain development in infants), Drs McDonald and Krainc of Northwestern University Feinberg School of Medicine find that this study highlights compelling evidence of the influence of the APOE e4 allele on brain structure in young infants. It remains to be determined whether these neurodevelopmental observations specifically influence AD pathogenesis in later life [<xref ref-type="bibr" rid="CIT0002">2</xref>]. In an editorial, Growdon JH, and Hyman BT allude to data emphasizing effects of B-amyloid on neural plasticity during brain development, a peptide elevated in Down syndrome where trisomy 21 leads to an extra copy of the amyloid precursor protein and early onset AZ [<xref ref-type="bibr" rid="CIT0003">3</xref>].</p>
<p>A study of effect of age and APOE genotype on neuropathological changes in Down syndrome hippocampal formation found that individuals who had inherited the APOE e4 genotype contained more than twice the amyloid burden of non-carriers. The level of amyloid deposition in Down syndrome patients is higher than in sporadic AZ disease [<xref ref-type="bibr" rid="CIT0004">4</xref>]. Inheritance of the APOE e4 genotype is an independent risk factor for developing higher levels of amyloid accumulation.</p>
</body>
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