【摘 要】
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Synaptic 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
【机 构】
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Department of Neurology, Renmin Hospital of Wuhan University, Wuhan,430060
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Synaptic 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 Ab-induced toxicity and promoted dendrite branching and synaptogenesis.Chronic oral administration of 7,8-DHF activated TrkB signaling and prevented Ab deposition in transgenic mice that coexpress five familial Alzheimers 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.Neuropsychopharmacology advance online publication, 2 October 2013;doi: 10.1038/npp.2013.243
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