| First Author | Sui Y | Year | 2019 |
| Journal | Brain Res | Volume | 1719 |
| Pages | 1-10 | PubMed ID | 31121157 |
| Mgi Jnum | J:282157 | Mgi Id | MGI:6380273 |
| Doi | 10.1016/j.brainres.2019.05.022 | Citation | Sui Y, et al. (2019) The small molecular CCR3 antagonist YM344031 attenuates neurodegenerative pathologies and improves learning and memory performance in a mouse model of Alzheimer's disease. Brain Res 1719:1-10 |
| abstractText | The chemokine C-C receptor 3 (CCR3) plays a role in the pathogenesis of Alzheimer's disease (AD). Based on our previous observations that deletion of CCR3 prevented neurodegenerative pathologies in amyloid precursor protein/presenilin 1 (APP/PS1) double-transgenic mice, we hypothesize that CCR3 antagonists may provide therapeutic benefits to AD. To this end, we examined the effect of the brain-penetrable CCR3 antagonist, YM344031, on AD-related pathologies in APP/PS1 double transgenic mice. Treatment of 10-month-old APP/PS1 double-transgenic mice with YM344031 (50mg/kg, b.i.d.) for two months resulted in dramatic decreases in beta-amyloid deposition, tau hyperphosphorylation and synaptic loss in the forebrain, significant attenuation of microgliosis and astrogliosis, and marked improvement of spatial learning and memory performance compared with the vehicle-treated mice. These results support CCR3 antagonism as a potential therapeutic strategy for AD. |
