Shati/Nat8l Overexpression Improves Cognitive Decline by Upregulating Neuronal Trophic Factor in Alzheimer’s Disease Model Mice

Kakeru Chino, Naotaka Izuo, Hiroshi Noike, Kyosuke Uno, Tomoharu Kuboyama, Chihiro Tohda, Shin Ichi Muramatsu, Atsumi Nitta*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

6 被引用数 (Scopus)

抄録

Alzheimer’s disease (AD) is a type of dementia characterized by the deposition of amyloid β, a causative protein of AD, in the brain. Shati/Nat8l, identified as a psychiatric disease related molecule, is a responsive enzyme of N-acetylaspartate (NAA) synthesis. In the hippocampi of AD patients and model mice, the NAA content and Shati/Nat8l expression were reported to be reduced. Having recently clarified the involvement of Shati/Nat8l in cognitive function, we examined the recovery effect of the hippocampal overexpression of Shati/Nat8l in AD model mice (5XFAD). Shati/Nat8l overexpression suppressed cognitive dysfunction without affecting the Aβ burden or number of NeuN-positive neurons. In addition, brain-derived neurotrophic factor mRNA was upregulated by Shati/Nat8l overexpression in 5XFAD mice. These results suggest that Shati/Nat8l overexpression prevents cognitive dysfunction in 5XFAD mice, indicating that Shati/Nat8l could be a therapeutic target for AD.

本文言語英語
ページ(範囲)2805-2814
ページ数10
ジャーナルNeurochemical Research
47
9
DOI
出版ステータス出版済み - 2022/09

ASJC Scopus 主題領域

  • 生化学
  • 細胞および分子神経科学

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