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.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Amyloid Precursor Protein Secretases / metabolism
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / drug effects
  • Animals
  • Aspartic Acid Endopeptidases / metabolism
  • Brain / drug effects*
  • Brain / metabolism
  • Disease Models, Animal
  • Memory / drug effects
  • Memory Disorders / drug therapy*
  • Mice, Transgenic
  • Neuroprotective Agents / pharmacology*

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Neuroprotective Agents
  • Amyloid Precursor Protein Secretases
  • Aspartic Acid Endopeptidases