4.5 Article

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

期刊

NEUROCHEMICAL RESEARCH
卷 47, 期 9, 页码 2805-2814

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-022-03649-2

关键词

Shati/Nat8l; Alzheimer's disease; Cognitive dysfunction; Amyloid beta; BDNF; AAV vector

资金

  1. Japan Society for the Promotion of Science [JSPS KAKENHI JP26293213, 21H02632, JP22H04922]
  2. Kobayashi Foundation
  3. SRF Grant for Biomedical Research and Foundation, Japan
  4. Grants-in-Aid for Scientific Research [21H02632] Funding Source: KAKEN

向作者/读者索取更多资源

Alzheimer's disease is characterized by the deposition of amyloid beta in the brain. Overexpression of Shati/Nat8l can prevent cognitive dysfunction in AD model mice, suggesting it as a potential therapeutic target for AD.
Alzheimer's disease (AD) is a type of dementia characterized by the deposition of amyloid beta, 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 A beta 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.

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