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7,8-Dihydroxyflavone Prevents Synaptic Loss and Memory Deficits in a Mouse Model of Alzheimer’s Disease
| Content Provider | Paperity |
|---|---|
| Author | Weinshenker, David Jason, P. Schroeder Ye, Keqiang Liu, Xia Zhang, Zhentao Song, Mingke Yu, Shan Ping Chan, Chi-bun |
| Abstract | 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 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. |
| Starting Page | 638 |
| Ending Page | 650 |
| File Format | HTM / HTML |
| DOI | 10.1038/npp.2013.243 |
| Journal | Neuropsychopharmacology |
| Volume Number | 39 |
| Language | English |
| Publisher | Nature Publishing Group |
| Publisher Date | 2013-09-11 |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
