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dc.contributor.authorKeowkase, Roongpetch
dc.contributor.authorAboukhatwa, Marwa
dc.contributor.authorAdam, Bao-Ling
dc.contributor.authorBeach, J Warren
dc.contributor.authorTerry, Alvin V.
dc.contributor.authorBuccafusco, Jerry J
dc.contributor.authorLuo, Yuan
dc.date.accessioned2012-10-26T16:26:54Z
dc.date.available2012-10-26T16:26:54Z
dc.date.issued2010-12-16en_US
dc.identifier.citationMol Neurodegener. 2010 Dec 16; 5:59en_US
dc.identifier.issn1750-1326en_US
dc.identifier.pmid21162742en_US
dc.identifier.doi10.1186/1750-1326-5-59en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/622
dc.description.abstractBackground: Our previous work indicated that novel analogs of choline have cytoprotective effects in vitro that might be useful in neurodegenerative conditions such as Alzheimer's disease (AD). Furthermore, two lead compounds (JWB1-84-1 and JAY2-22-33) from a library of more than 50 improved cognitive performances in a transgenic mouse model of AD. The purpose of these experiments was to more specifically investigate the neuroprotective capabilities of these lead compounds both in vitro and in vivo.
dc.description.abstractResults: We used N2a cells which express a Swedish mutation in the amyloid precursor protein and presenilin 1 genes to investigate the effect of JWB1-84-1 and JAY2-22-33 on b-amyloid (Ab) levels and found that both compounds significantly reduced Ab levels. JWB1-84-1 and JAY2-22-33 also protected rat primary cortical neurons from Ab toxicity. Subsequently, we utilized the nematode Caenorhabditis elegans (C. elegans) as an in vivo model organism to identify potential molecular targets of these compounds. In the C. elegans model of Ab toxicity, human Ab is expressed intracellularly in the body wall muscle. The expression and subsequent aggregation of Ab in the muscle leads to progressive paralysis.
dc.description.abstractConclusion: We found that JAY2-22-33 (but not JWB1-84-1) significantly reduced Ab toxicity by delaying paralysis and this protective effect required both the insulin signaling pathway and nicotinic acetylcholine receptors (nAChRs).
dc.rightsCopyright ©2010 Keowkase et al; licensee BioMed Central Ltd.en_US
dc.subjectResearch Articleen_US
dc.titleNeuroprotective effects and mechanism of cognitive-enhancing choline analogs JWB 1-84-1 and JAY 2-22-33 in neuronal culture and Caenorhabditis elegansen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3017027en_US
dc.contributor.corporatenameDepartment of Pharmacology and Toxicology
refterms.dateFOA2019-04-10T09:13:56Z
html.description.abstractBackground: Our previous work indicated that novel analogs of choline have cytoprotective effects in vitro that might be useful in neurodegenerative conditions such as Alzheimer's disease (AD). Furthermore, two lead compounds (JWB1-84-1 and JAY2-22-33) from a library of more than 50 improved cognitive performances in a transgenic mouse model of AD. The purpose of these experiments was to more specifically investigate the neuroprotective capabilities of these lead compounds both in vitro and in vivo.
html.description.abstractResults: We used N2a cells which express a Swedish mutation in the amyloid precursor protein and presenilin 1 genes to investigate the effect of JWB1-84-1 and JAY2-22-33 on b-amyloid (Ab) levels and found that both compounds significantly reduced Ab levels. JWB1-84-1 and JAY2-22-33 also protected rat primary cortical neurons from Ab toxicity. Subsequently, we utilized the nematode Caenorhabditis elegans (C. elegans) as an in vivo model organism to identify potential molecular targets of these compounds. In the C. elegans model of Ab toxicity, human Ab is expressed intracellularly in the body wall muscle. The expression and subsequent aggregation of Ab in the muscle leads to progressive paralysis.
html.description.abstractConclusion: We found that JAY2-22-33 (but not JWB1-84-1) significantly reduced Ab toxicity by delaying paralysis and this protective effect required both the insulin signaling pathway and nicotinic acetylcholine receptors (nAChRs).


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