JBPOS0101 attenuates amyloid-β accumulation and memory loss in a mouse model of Alzheimer's disease

  • Neuroreport. 2019 Jul 3;30(10):741-747. doi: 10.1097/WNR.0000000000001269.
Hyung Joon Park  1 ,  Ju Kyong Jang  2 ,  Yong Moon Choi  2 ,  Won-Seok Choi  1
Affiliations
  • 1. School of Biological Sciences and Technology, College of Natural Sciences, College of Medicine, Chonnam National University, Gwangju.
  • 2. Bio-Pharm Solutions Co. Ltd, Suwon, Gyeonggi-Do, Republic of Korea.
PMID: 31095107 DOI: 10.1097/WNR.0000000000001269
Abstract

Alzheimer's disease (AD) is a major neurodegenerative disorder characterized by the accumulation of Amyloid-β (Aβ) in the brain. Defects in Aβ clearance or the interference of Aβ homeostasis could result in Aβ aggregation. JBPOS0101 has been studied for its antiepileptic activity. It showed a neuroprotective effect and prevented memory deficits in lithium-pilocarpine-induced status epilepticus rats. In this study, we tested the effect of JBPOS0101 in an AD model. We showed that JBPOS0101 attenuated the accumulation of Aβ in 5XFAD mouse brains. Moreover, the treatment of JBPOS0101 rescued the deficits in learning and memory in 5XFAD mice. These data suggest that JBPOS0101 could be a potential therapeutic drug candidate for AD.

Products