期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 61, 期 1, 页码 259-263出版社
IOS PRESS
DOI: 10.3233/JAD-170645
关键词
Amyloid beta; ASK1; brain aging; cognitive function; vascular injury
资金
- Astellas
- AstraZeneca
- Boehringer Ingelheim
- Daiichi Sankyo
- Novartis
- Shionogi
- Takeda
- Kyowa Hakko Kirin
- Grants-in-Aid for Scientific Research [16K15115] Funding Source: KAKEN
To examine the role of ASK1 in Alzheimer's disease (AD), we generated 5XFAD mice deficient in ASK1 and investigated the characteristics of old 5XFADand wild-type mice with ASK1 deficiency. ASK1 deficiency improved cognitive function in 24-month-old 5XFAD mice, which was associated with the reduction of phosphorylated p38. Thus, ASK1/p38 cascade seems to play some role in the pathogenesis of AD in mice. In 24-month-old wild-type mice, ASK1 deficiency increased cerebral vasoreactivity to acetazolamide and significantly reduced brain soluble A beta, which were also associated with the reduction of phosphorylated p38. Thus, ASK1/p38 cascade may contribute to brain aging of wild-type mice. Collectively, our present results provided the evidence suggesting the involvement of ASK1/p38 cascade in AD and brain aging.
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