Targeting the JAK2/STAT3 axis in Alzheimer's disease

Tomohiro Chiba, Marina Yamada, Sadakazu Aiso

研究成果: Review article査読

68 被引用数 (Scopus)

抄録

Background: Amyloid aβ (Aaβ) has long been implicated in the pathogenesis of Alzheimer's disease (AD). Little is known, however, about the intracellular events in neurons which lead to memory loss related to AD. Focusing on the fact that an AD-specific neuroprotective peptide named humanin (HN) inhibits AD-related neurotoxicity by activating the JAK2/STAT3 signaling axis, we recently found that age- and disease-dependent deterioration in the JAK2/STAT3 axis plays a critical role in the pathogenesis of AD. Objective/methods: Here we summarize the neuroprotective effect of HN and its derivative, named colivelin (CLN), and also review the roles of the JAK2/STAT3 axis in memory impairment related to AD. Results/conclusions: The JAK2/STAT3 axis is a major transducer of HN-mediated neuroprotective activity. Aâ-dependent inactivation of the JAK2/STAT3 axis in hippocampal neurons causes cholinergic dysfunction via pre- and post-synaptic mechanisms, which leads to memory impairment related to AD. This provides not only a novel pathological hallmark of AD but also a novel target in AD therapy.

本文言語English
ページ(範囲)1155-1167
ページ数13
ジャーナルExpert Opinion on Therapeutic Targets
13
10
DOI
出版ステータスPublished - 2009 10
外部発表はい

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery
  • Clinical Biochemistry

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