Affiliations: [a] Department of Internal Medicine, Gerontology & Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA
| [b] Department of Physiology and Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC, USA
| [c] Department of Neurobiology and Anatomy, Wake Forest School of Medicine, Winston-Salem, NC, USA
Correspondence:
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Correspondence to: Dr. Tao Ma, Department of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. Tel.: +1 336 7164981; Fax: +1 336 7138826; E-mail: [email protected].
Abstract: 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.
Keywords: Alzheimer’s disease, AMPK, protein synthesis, signaling transduction, synaptic plasticity
