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The stress response factor FOXO3 is neuroprotective in models of Huntington\u2019s disease (HD), Parkinson\u2019s disease and motor-neuron diseases. Neuroprotective compounds acting in a FOXO-dependent manner could thus constitute <jats:italic>bona fide<\/jats:italic> drugs for promoting neuronal compensation. However, whether FOXO-dependent neuroprotection is a common feature of several compound families remains unknown. Using drug screening in <jats:italic>C. elegans<\/jats:italic> nematodes with neuronal expression of human exon-1 huntingtin (128Q), we found that 3\u00df-Methoxy-Pregnenolone (MAP4343), 17\u00df-oestradiol (17\u00dfE2) and 12 flavonoids including isoquercitrin promote neuronal function in 128Q nematodes. MAP4343, 17\u00dfE2 and isoquercitrin also promote stress resistance in mutant <jats:italic>Htt<\/jats:italic> striatal cells derived from knock-in HD mice. Interestingly, <jats:italic>daf-16<\/jats:italic>\/FOXO is required for MAP4343, 17\u00dfE2 and isoquercitrin to sustain neuronal function in 128Q nematodes. This similarly applies to the GSK3 inhibitor lithium chloride (LiCl) and, as previously described, to resveratrol and the AMPK activator metformin. Daf-16\/FOXO and the targets engaged by these compounds define a sub-network enriched for stress-response and neuronally-active pathways. Collectively, these data highlights the dependence on a <jats:italic>daf-16<\/jats:italic>\/FOXO-interaction network as a common feature of several compound families for prolonging neuronal function in HD.<\/jats:p>","DOI":"10.1038\/s41598-017-04256-w","type":"journal-article","created":{"date-parts":[[2017,6,15]],"date-time":"2017-06-15T20:45:58Z","timestamp":1497559558000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["The stress response factor daf-16\/FOXO is required for multiple compound families to prolong the function of neurons with Huntington\u2019s disease"],"prefix":"10.1038","volume":"7","author":[{"given":"Francesca","family":"Farina","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuel","family":"Lambert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucie","family":"Commeau","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7ois-Xavier","family":"Lejeune","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathalie","family":"Roudier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cosima","family":"Fonte","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3333-2445","authenticated-orcid":false,"given":"J. Alex","family":"Parker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Boddaert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Verny","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Etienne-Emile","family":"Baulieu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Neri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,6,21]]},"reference":[{"key":"4256_CR1","doi-asserted-by":"publisher","first-page":"709","DOI":"10.1016\/j.cell.2014.10.039","volume":"159","author":"BK Kennedy","year":"2014","unstructured":"Kennedy, B. K. et al. Geroscience: linking aging to chronic disease. 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