Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 68, Issue 1, Pages 33-38Publisher
IOS PRESS
DOI: 10.3233/JAD-181043
Keywords
Alzheimer's disease; AMPK; protein synthesis; signaling transduction; synaptic plasticity
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Funding
- National Institutes of Health [K99/R00 AG044469, R01 AG055581, R01 AG056622, F31AG055264]
- Alzheimer's Association [NIRG-15-362799]
- BrightFocus Foundation [A2017457S]
- Wake Forest Alzheimer's Disease Research Center (ADRC) [P30AG049638]
- Wake Forest Clinical and Translational Science Institute (CTSI)
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Currently there is no cure or effective disease-modifying therapy for Alzheimer's disease (AD), the most common form of dementia that is becoming a global threat to public health. It is important to develop novel therapeutic strategies targeting AD pathophysiology particularly synaptic failure and cognitive impairments. Recent studies revealed several molecular signaling pathways potentially linked to brain pathology and synaptic failure in AD, including AMP-activated protein kinase (AMPK), a master kinase that plays a central role in the maintenance of cellular energy homeostasis. Particularly, hyperactive AMPK via phosphorylation has been linked to AD-associated synaptic plasticity impairments, indicating suppression of AMPK activity might be beneficial for cognitive deficiency in AD. In this review, we will discuss how targeting dysregulation of AMPK signaling could be a feasible therapeutic approach for AD.
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