Apoptosis Signal Regulating Kinase 1 (ASK1): Potential as a Therapeutic Target for Alzheimer’s Disease

International Journal of Molecular Sciences

Juhyun Song¹  Kyung Ah Park¹  Won Taek Lee¹ 

[1] Department of Anatomy, Yonsei University College of Medicine, Seoul 120-752, Korea; E-Mails:

关键词: apoptosis signal regulating kinase 1 (ASK1);    Alzheimer’s disease (AD);    oxidative stress;    endoplasmic reticulum (ER) stress;    Aβ neurotoxicity;    tau protein phosphorylation;    insulin signal transduction;   

DOI  :  10.3390/ijms15022119

来源: mdpi

【 摘 要 】

Alzheimer’s disease (AD) is the most common form of dementia, characterized by a decline in memory and cognitive function. Clinical manifestations of AD are closely associated with the formation of senile plaques and neurofibrillary tangles, neuronal loss and cognitive decline. Apoptosis signal regulating kinase 1 (ASK1) is a mediator of the MAPK pathway, which regulates various cellular responses such as apoptosis, cell survival, and differentiation. Accumulating evidence indicates that ASK1 plays a key role in the pathogenesis of neurodegenerative disorders such as Huntington’s disease and AD. Of particular interest, ASK1 is associated with many signaling pathways, which include endoplasmic reticulum (ER) stress-mediated apoptosis, Aβ-induced neurotoxicity, tau protein phosphorylation, and insulin signal transduction. Here, we review experimental evidence that links ASK1 signaling and AD pathogenesis and propose that ASK1 might be a new point of therapeutic intervention to prevent or treat AD.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland