Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 15, Issue 2, Pages 2119-2129Publisher
MDPI
DOI: 10.3390/ijms15022119
Keywords
apoptosis signal regulating kinase 1 (ASK1); Alzheimer's disease (AD); oxidative stress; endoplasmic reticulum (ER) stress; A neurotoxicity; tau protein phosphorylation; insulin signal transduction
Funding
- National Research Foundation of Korea (NRF) - Korean government (MEST) [2011-0017276]
- Brain Korea 21 Plus Project for Medical Science, Yonsei University
- National Research Foundation of Korea [2011-0017276] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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, A-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.
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