Nobiletin restoring β-amyloid-impaired CREB phosphorylation rescues memory deterioration in Alzheimer's disease model rats

Kentaro Matsuzaki, Tohru Yamakuni, Michio Hashimoto, Abdul Md Haque, Osamu Shido, Yoshihiro Mimaki, Yutaka Sashida, Yasushi Ohizumi

研究成果: Article査読

108 被引用数 (Scopus)

抄録

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive and memory deterioration. Production and accumulation of β-amyloid peptide (Aβ) is central to the pathogenesis of AD. Recent studies have demonstrated that PKA/CREB-dependent signaling pathway and long-term potentiation are inhibited by sublethal concentrations of Aβ1-42 in cultured hippocampus neurons. Here, we examined the effects of nobiletin on the Aβ-induced inhibition of CREB phosphorylation in cultured rat hippocampus neurons. A sublethal concentration of Aβ1-42 or Aβ1-40 decreased glutamate-induced CREB phosphorylation, whereas pretreatment with nobiletin reversed the Aβ-induced decrease in CREB phosphorylation. The effects of nobiletin on impairment of learning ability were also examined in chronically Aβ1-40 infused AD model rats using the eight-arm radial maze. In the AD model rats, nobiletin showed protective effects on Aβ1-40-induced impairment of learning ability. These results suggest that nobiletin has the potential for becoming a novel lead compound for drug development for AD.

本文言語English
ページ(範囲)230-234
ページ数5
ジャーナルNeuroscience Letters
400
3
DOI
出版ステータスPublished - 2006 6 12

ASJC Scopus subject areas

  • Neuroscience(all)

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