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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic>
</title>
<author><name sortKey="Muffat, Julien" sort="Muffat, Julien" uniqKey="Muffat J" first="Julien" last="Muffat">Julien Muffat</name>
<affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="aff2">University of Paris VI Pierre et Marie Curie, Paris 75006, France</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Walker, David W" sort="Walker, David W" uniqKey="Walker D" first="David W." last="Walker">David W. Walker</name>
<affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Benzer, Seymour" sort="Benzer, Seymour" uniqKey="Benzer S" first="Seymour" last="Benzer">Seymour Benzer</name>
<affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">18458334</idno>
<idno type="pmc">2374552</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374552</idno>
<idno type="RBID">PMC:2374552</idno>
<idno type="doi">10.1073/pnas.0800896105</idno>
<date when="2008">2008</date>
<idno type="wicri:Area/Pmc/Corpus">000531</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000531</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic>
</title>
<author><name sortKey="Muffat, Julien" sort="Muffat, Julien" uniqKey="Muffat J" first="Julien" last="Muffat">Julien Muffat</name>
<affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="aff2">University of Paris VI Pierre et Marie Curie, Paris 75006, France</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Walker, David W" sort="Walker, David W" uniqKey="Walker D" first="David W." last="Walker">David W. Walker</name>
<affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Benzer, Seymour" sort="Benzer, Seymour" uniqKey="Benzer S" first="Seymour" last="Benzer">Seymour Benzer</name>
<affiliation><nlm:aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title>
<idno type="ISSN">0027-8424</idno>
<idno type="eISSN">1091-6490</idno>
<imprint><date when="2008">2008</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Apolipoprotein D (ApoD) expression increases in several neurological disorders and in spinal cord injury. We provide a report of a physiological role for human ApoD (hApoD): Flies overexpressing hApoD are long-lived and protected against stress conditions associated with aging and neurodegeneration, including hyperoxia, dietary paraquat, and heat stress. We show that the fly ortholog, <italic>Glial Lazarillo</italic>
, is strongly up-regulated in response to these extrinsic stresses and also can protect <italic>in vitro</italic>
-cultured cells in situations modeling Alzheimer's disease (AD) and Parkinson's disease (PD). In adult flies, hApoD overexpression reduces age-associated lipid peroxide accumulation, suggesting a proximal mechanism of action. Similar data obtained in the mouse [Ganfornina, M.D., <italic>et al.</italic>
, (2008) Apolipoprotein D is involved in the mechanisms regulating protection from oxidative stress. <italic>Aging Cell</italic>
10.1111/j.1474-9726.2008.00395.] as well as in plants (Charron <italic>et al.</italic>
, personal communication) suggest that ApoD and its orthologs play an evolutionarily conserved role in response to stress, possibly managing or preventing lipid peroxidation.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id>
<journal-id journal-id-type="hwp">pnas</journal-id>
<journal-id journal-id-type="pmc">pnas</journal-id>
<journal-id journal-id-type="publisher-id">PNAS</journal-id>
<journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title>
</journal-title-group>
<issn pub-type="ppub">0027-8424</issn>
<issn pub-type="epub">1091-6490</issn>
<publisher><publisher-name>National Academy of Sciences</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">18458334</article-id>
<article-id pub-id-type="pmc">2374552</article-id>
<article-id pub-id-type="publisher-id">0429</article-id>
<article-id pub-id-type="doi">10.1073/pnas.0800896105</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject>
<subj-group><subject>Physiology</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Human ApoD, an apolipoprotein up-regulated in neurodegenerative diseases, extends lifespan and increases stress resistance in <italic>Drosophila</italic>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Muffat</surname>
<given-names>Julien</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="aff" rid="aff2"><sup>†</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>‡</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Walker</surname>
<given-names>David W.</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="corresp" rid="cor1"><sup>‡</sup>
</xref>
<xref ref-type="author-notes" rid="FN1"><sup>§</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Benzer</surname>
<given-names>Seymour</given-names>
</name>
<xref ref-type="aff" rid="aff1">*</xref>
<xref ref-type="author-notes" rid="FN2"><sup>¶</sup>
</xref>
</contrib>
<aff id="aff1">*Division of Biology, California Institute of Technology, Pasadena, CA 91125; and</aff>
<aff id="aff2"><sup>†</sup>
University of Paris VI Pierre et Marie Curie, Paris 75006, France</aff>
</contrib-group>
<author-notes><corresp id="cor1"><sup>‡</sup>
To whom correspondence may be addressed. E-mail: <email>julien@caltech.edu</email>
or <email>davidwalker@ucla.edu</email>
</corresp>
<fn fn-type="con"><p>Contributed by Seymour Benzer, March 26, 2008</p>
</fn>
<fn fn-type="con"><p>Author contributions: J.M., D.W.W., and S.B. designed research; J.M. performed research; J.M. contributed new reagents/analytic tools; J.M. and D.W.W. analyzed data; and J.M., D.W.W., and S.B. wrote the paper.</p>
</fn>
<fn fn-type="present-address" id="FN1"><p><sup>§</sup>
Present address: Department of Physiological Science, University of California, Los Angeles, CA 90095.</p>
</fn>
<fn fn-type="deceased" id="FN2"><p><sup>¶</sup>
Deceased November 30, 2007.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><day>13</day>
<month>5</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="epub"><day>5</day>
<month>5</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>5</day>
<month>5</month>
<year>2008</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
epub date downloaded from Highwire. </pmc-comment>
<volume>105</volume>
<issue>19</issue>
<fpage>7088</fpage>
<lpage>7093</lpage>
<history><date date-type="received"><day>1</day>
<month>10</month>
<year>2007</year>
</date>
</history>
<permissions><copyright-statement>© 2008 by The National Academy of Sciences of the USA</copyright-statement>
<license license-type="open-access"><license-p>Freely available online through the PNAS open access option.</license-p>
</license>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zpq01908007088.pdf"></self-uri>
<abstract><p>Apolipoprotein D (ApoD) expression increases in several neurological disorders and in spinal cord injury. We provide a report of a physiological role for human ApoD (hApoD): Flies overexpressing hApoD are long-lived and protected against stress conditions associated with aging and neurodegeneration, including hyperoxia, dietary paraquat, and heat stress. We show that the fly ortholog, <italic>Glial Lazarillo</italic>
, is strongly up-regulated in response to these extrinsic stresses and also can protect <italic>in vitro</italic>
-cultured cells in situations modeling Alzheimer's disease (AD) and Parkinson's disease (PD). In adult flies, hApoD overexpression reduces age-associated lipid peroxide accumulation, suggesting a proximal mechanism of action. Similar data obtained in the mouse [Ganfornina, M.D., <italic>et al.</italic>
, (2008) Apolipoprotein D is involved in the mechanisms regulating protection from oxidative stress. <italic>Aging Cell</italic>
10.1111/j.1474-9726.2008.00395.] as well as in plants (Charron <italic>et al.</italic>
, personal communication) suggest that ApoD and its orthologs play an evolutionarily conserved role in response to stress, possibly managing or preventing lipid peroxidation.</p>
</abstract>
<kwd-group><kwd>aging</kwd>
<kwd>Alzheimer</kwd>
<kwd>β-amyloid</kwd>
<kwd>GLaz</kwd>
<kwd>oxidative stress</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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