{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T07:57:33Z","timestamp":1792396653070,"version":"4.4.0"},"reference-count":70,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2008,1,16]],"date-time":"2008-01-16T00:00:00Z","timestamp":1200441600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:p>\n                    Intracellular antibodies (intrabodies) and the chaperone, heat shock protein 70 (Hsp70), have each shown potential as therapeutics for neurode generative diseases\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo.<\/jats:italic>\n                    Investigating combinational therapy in an established\n                    <jats:italic>Drosophila<\/jats:italic>\n                    model of Huntington's disease (HD), we show that Hsp70 and intrabody actually affect different aspects of the disease. Overexpression of human Hsp70 re sulted in improved survival of HD flies to eclosion and prolonged adult life compared with intrabody treat ment alone. An additive effect on adult survival was observed when the two therapies were combined. Intra body was more successful at suppressing neurodegen eration in photoreceptors than was Hsp70. Further more, Hsp70 treatment alone did not block aggregation of mutant huntingtin, a process slowed by intrabody. Expression of each is restricted to the nervous system, which implies different neuronal populations respond distinctly to these treatments. Importantly, a role for endogenous Hsp70 in suppression of mutant hunting\u2010tin pathology was confirmed by a separate set of genetic studies in which HD flies deficient for Hsp70 showed significantly increased pathology. We conclude that a combinational approach of intrabody with enhanced Hsp70 expression is beneficial in addressing multiple pathologies associated with HD and has potential ap plication for other neurodegenerative disorders.\u2014 McLear, J. A., Lebrecht, D., Messer, A., Wolfgang, W. J. Combinational approach of intrabody with enhanced Hsp70 expression addresses multiple pathologies in a fly model of Huntington's disease.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    22, 2003\u20132011 (2008)\n                  <\/jats:p>","DOI":"10.1096\/fj.07-099689","type":"journal-article","created":{"date-parts":[[2008,1,16]],"date-time":"2008-01-16T20:34:43Z","timestamp":1200515683000},"page":"2003-2011","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Combinational approach of intrabody with enhanced Hsp70 expression addresses multiple pathologies in a fly model of Huntington's disease"],"prefix":"10.1096","volume":"22","author":[{"given":"J. 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