| First Author | Teich AF | Year | 2018 |
| Journal | Alzheimers Dement (N Y) | Volume | 4 |
| Pages | 37-45 | PubMed ID | 29955650 |
| Mgi Jnum | J:351926 | Mgi Id | MGI:7703867 |
| Doi | 10.1016/j.trci.2017.12.001 | Citation | Teich AF, et al. (2018) Translational inhibition of APP by Posiphen: Efficacy, pharmacodynamics, and pharmacokinetics in the APP/PS1 mouse. Alzheimers Dement (N Y) 4:37-45 |
| abstractText | INTRODUCTION: Translational inhibition of amyloid precursor protein (APP) by Posiphen has been shown to reduce APP and its fragments in cell culture, animal models, and mildly cognitively impaired patients, making it a promising drug candidate for the treatment of Alzheimer's disease. METHODS: We used a mouse model of Alzheimer's disease (APP/presenilin-1) to examine Posiphen's efficacy, pharmacodynamics, and pharmacokinetics. RESULTS: Posiphen treatment normalized impairments in spatial working memory, contextual fear learning, and synaptic function in APP/presenilin-1 mice, without affecting their visual acuity, motor skills, or motivation and without affecting wild-type mice. Posiphen had a prolonged effect in reducing APP and all related peptides for at least 9 hours after the last dose. Its concentration was higher in the brain than in plasma, and the most abundant metabolite was N(8)-norPosiphen. DISCUSSION: This is the first study demonstrating the therapeutic efficacy of inhibiting the translation of APP and its fragments in an Alzheimer's disease model. |
