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Article: 7,8-dihydroxyflavone prevents synaptic loss and memory deficits in a mouse model of Alzheimer's disease

Title7,8-dihydroxyflavone prevents synaptic loss and memory deficits in a mouse model of Alzheimer's disease
Authors
Keywords7,8-Dihydroxyflavone
Alzheimer's disease
TrkB
Synapse
neuroprotection
Issue Date2014
Citation
Neuropsychopharmacology, 2014, v. 39, n. 3, p. 638-650 How to Cite?
AbstractSynaptic loss in the brain correlates well with disease severity in Alzheimer disease (AD). Deficits in brain-derived neurotrophic factor/tropomyosin-receptor-kinase B (TrkB) signaling contribute to the synaptic dysfunction of AD. We have recently identified 7,8-dihydroxyflavone (7,8-DHF) as a potent TrkB agonist that displays therapeutic efficacy toward various neurological diseases. Here we tested the effect of 7,8-DHF on synaptic function in an AD model both in vitro and in vivo. 7,8-DHF protected primary neurons from Aβ-induced toxicity and promoted dendrite branching and synaptogenesis. Chronic oral administration of 7,8-DHF activated TrkB signaling and prevented Aβ deposition in transgenic mice that coexpress five familial Alzheimer's disease mutations (5XFAD mice). Moreover, 7,8-DHF inhibited the loss of hippocampal synapses, restored synapse number and synaptic plasticity, and prevented memory deficits. These results suggest that 7,8-DHF represents a novel oral bioactive therapeutic agent for treating AD. © 2014 American College of Neuropsychopharmacology.
Persistent Identifierhttp://hdl.handle.net/10722/225058
ISSN
2015 Impact Factor: 6.399
2015 SCImago Journal Rankings: 3.517

 

DC FieldValueLanguage
dc.contributor.authorZhang, Zhentao-
dc.contributor.authorLiu, Xia-
dc.contributor.authorSchroeder, Jason P.-
dc.contributor.authorChan, Chi Bun-
dc.contributor.authorSong, Mingke-
dc.contributor.authorYu, Shan Ping-
dc.contributor.authorWeinshenker, David-
dc.contributor.authorYe, Keqiang-
dc.date.accessioned2016-04-18T11:16:39Z-
dc.date.available2016-04-18T11:16:39Z-
dc.date.issued2014-
dc.identifier.citationNeuropsychopharmacology, 2014, v. 39, n. 3, p. 638-650-
dc.identifier.issn0893-133X-
dc.identifier.urihttp://hdl.handle.net/10722/225058-
dc.description.abstractSynaptic loss in the brain correlates well with disease severity in Alzheimer disease (AD). Deficits in brain-derived neurotrophic factor/tropomyosin-receptor-kinase B (TrkB) signaling contribute to the synaptic dysfunction of AD. We have recently identified 7,8-dihydroxyflavone (7,8-DHF) as a potent TrkB agonist that displays therapeutic efficacy toward various neurological diseases. Here we tested the effect of 7,8-DHF on synaptic function in an AD model both in vitro and in vivo. 7,8-DHF protected primary neurons from Aβ-induced toxicity and promoted dendrite branching and synaptogenesis. Chronic oral administration of 7,8-DHF activated TrkB signaling and prevented Aβ deposition in transgenic mice that coexpress five familial Alzheimer's disease mutations (5XFAD mice). Moreover, 7,8-DHF inhibited the loss of hippocampal synapses, restored synapse number and synaptic plasticity, and prevented memory deficits. These results suggest that 7,8-DHF represents a novel oral bioactive therapeutic agent for treating AD. © 2014 American College of Neuropsychopharmacology.-
dc.languageeng-
dc.relation.ispartofNeuropsychopharmacology-
dc.subject7,8-Dihydroxyflavone-
dc.subjectAlzheimer's disease-
dc.subjectTrkB-
dc.subjectSynapse-
dc.subjectneuroprotection-
dc.title7,8-dihydroxyflavone prevents synaptic loss and memory deficits in a mouse model of Alzheimer's disease-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1038/npp.2013.243-
dc.identifier.pmid24022672-
dc.identifier.scopuseid_2-s2.0-84892680431-
dc.identifier.volume39-
dc.identifier.issue3-
dc.identifier.spage638-
dc.identifier.epage650-
dc.identifier.eissn1740-634X-

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