| First Author | Hong X | Year | 2014 |
| Journal | Hum Mol Genet | Volume | 23 |
| Issue | 4 | Pages | 1056-72 |
| PubMed ID | 24105468 | Mgi Jnum | J:205991 |
| Mgi Id | MGI:5547635 | Doi | 10.1093/hmg/ddt501 |
| Citation | Hong X, et al. (2014) Parkin overexpression ameliorates hippocampal long-term potentiation and beta-amyloid load in an Alzheimer's disease mouse model. Hum Mol Genet 23(4):1056-72 |
| abstractText | Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a severe decline of memory performance. A widely studied AD mouse model is the APPswe/PSEN1DeltaE9 (APP/PS1) strain, as mice exhibit amyloid plaques as well as impaired memory capacities. To test whether restoring synaptic plasticity and decreasing beta-amyloid load by Parkin could represent a potential therapeutic target for AD, we crossed APP/PS1 transgenic mice with transgenic mice overexpressing the ubiquitin ligase Parkin and analyzed offspring properties. Overexpression of Parkin in APP/PS1 transgenic mice restored activity-dependent synaptic plasticity and rescued behavioral abnormalities. Moreover, overexpression of Parkin was associated with down-regulation of APP protein expression, decreased beta-amyloid load and reduced inflammation. Our data suggest that Parkin could be a promising target for AD therapy. |
