<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Basic and Clinical Neuroscience Journal</title>
<title_fa>مجله علوم اعصاب پایه و بالینی</title_fa>
<short_title>BCN</short_title>
<subject>Medical Sciences</subject>
<web_url>http://bcn.iums.ac.ir</web_url>
<journal_hbi_system_id>137</journal_hbi_system_id>
<journal_hbi_system_user>journal137</journal_hbi_system_user>
<journal_id_issn>2008-126X</journal_id_issn>
<journal_id_issn_online>2228-7442</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi>10.32598/bcn</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid></journal_id_sid>
<journal_id_nlai></journal_id_nlai>
<journal_id_science></journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1396</year>
	<month>12</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2018</year>
	<month>3</month>
	<day>1</day>
</pubdate>
<volume>0</volume>
<number>Accepted Articles</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>The Possible Relationship Between the APOE4 Isoform and White Matter Loss in Multiple Sclerosis Patients: An Exploratory Study</title>
	<subject_fa>Cellular and molecular Neuroscience</subject_fa>
	<subject>Cellular and molecular Neuroscience</subject>
	<content_type_fa>Original</content_type_fa>
	<content_type>Original</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;div style=&quot;text-align: justify;&quot;&gt;&lt;span style=&quot;font-size:14px;&quot;&gt;&lt;span style=&quot;font-family:Tahoma;&quot;&gt;&lt;span style=&quot;line-height:2;&quot;&gt;&lt;b&gt;Background:&lt;/b&gt; Apolipoprotein E (APOE) is crucial for neuronal maintenance and myelin repair. The APOE4 isoform is associated with an increased risk of neurodegeneration in multiple sclerosis patients. This study investigated the association between APOE polymorphisms and brain atrophy in multiple sclerosis patients.&lt;br&gt;
&lt;b&gt;Methods:&lt;/b&gt; The current cross-sectional study was performed on 70 relapsing-remitting multiple sclerosis (RRMS) patients, evaluating two common missense APOE polymorphisms, rs429358 and rs7412, in all participants. The FreeSurfer software measured whole-brain volume by analyzing T1-weighted Magnetic Resonance Imaging (MRI) sequences. &lt;span style=&quot;font-family:&amp;quot;Times New Roman&amp;quot;,serif&quot;&gt;&lt;/span&gt;&lt;br&gt;
Diffusion tensor imaging (DTI) data were preprocessed with MRtrix3 and analyzed using FSL.&lt;br&gt;
&lt;b&gt;Results:&lt;/b&gt; Patients with APOE4 exhibited lower white matter (WM) volume than those without this isoform (274.25&amp;plusmn;32.20, vs. 307.51&amp;plusmn;36.36, p=0.02). After adjusting for confounding factors, there was a significant association between APOE4 and lower WM volume (p=0.03, partial Eta square (&lt;i&gt;&amp;eta;&amp;sup2;&lt;/i&gt;) = 0.08). Indeed, a negative independent association was found between disease duration and WM volume (p = 0.02, &lt;i&gt;&amp;eta;&amp;sup2;&lt;/i&gt; = 0.09).&lt;br&gt;
DTI data were analyzed in 7 APOE4 carriers and 8 non-carriers matched for age, sex, and MS duration.&amp;nbsp; FA in WM (1.75(0.13), vs. 1.83 (0.18)) and corpus callosum (2.09(0.78), vs. 2.21(0.30)) were lower in APOE4 carriers, but not significantly (p&gt;0.05).&lt;br&gt;
&lt;b&gt;Conclusion: &lt;/b&gt;The present study&lt;i&gt; &lt;/i&gt;suggested a potential genetic influence of APOE4 on brain WM atrophy, specifically the corpus callosum, in MS patients.&lt;/span&gt;&lt;/span&gt;&lt;/span&gt;&lt;/div&gt;</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Multiple sclerosis, brain mapping, white matter atrophy, APOE ​​​​​​​</keyword>
	<start_page>0</start_page>
	<end_page>0</end_page>
	<web_url>http://bcn.iums.ac.ir/browse.php?a_code=A-10-8523-1&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Zhila</first_name>
	<middle_name></middle_name>
	<last_name>Maghbooli</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>zhilayas@gmail.com</email>
	<code>13700319475328460058190</code>
	<orcid>13700319475328460058190</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Multiple Sclerosis Research Center, Neurosciences Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Sajad</first_name>
	<middle_name></middle_name>
	<last_name>Sahab Negah</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>sahabsajad@yahoo.com</email>
	<code>13700319475328460058191</code>
	<orcid>13700319475328460058191</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Multiple Sclerosis Research Center, Neurosciences Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohammad Ali</first_name>
	<middle_name></middle_name>
	<last_name>Sahraian</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>sahraian1350@yahoo.com</email>
	<code>13700319475328460058192</code>
	<orcid>13700319475328460058192</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Multiple Sclerosis Research Center, Neurosciences Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
