| First Author | Kim HY | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 8997 | PubMed ID | 26646366 |
| Mgi Jnum | J:228875 | Mgi Id | MGI:5749592 |
| Doi | 10.1038/ncomms9997 | Citation | Kim HY, et al. (2015) EPPS rescues hippocampus-dependent cognitive deficits in APP/PS1 mice by disaggregation of amyloid-beta oligomers and plaques. Nat Commun 6:8997 |
| abstractText | Alzheimer's disease (AD) is characterized by the transition of amyloid-beta (Abeta) monomers into toxic oligomers and plaques. Given that Abeta abnormality typically precedes the development of clinical symptoms, an agent capable of disaggregating existing Abeta aggregates may be advantageous. Here we report that a small molecule, 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS), binds to Abeta aggregates and converts them into monomers. The oral administration of EPPS substantially reduces hippocampus-dependent behavioural deficits, brain Abeta oligomer and plaque deposits, glial gamma-aminobutyric acid (GABA) release and brain inflammation in an Abeta-overexpressing, APP/PS1 transgenic mouse model when initiated after the development of severe AD-like phenotypes. The ability of EPPS to rescue Abeta aggregation and behavioural deficits provides strong support for the view that the accumulation of Abeta is an important mechanism underlying AD. |
