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Highlighting the Protective or Degenerative Role of AMPK Activators in Dementia Experimental Models

[ Vol. 20 , Issue. 9 ]

Author(s):

Marjan Nikbakhtzadeh, Fatemeh Shaerzadeh and Ghorbangol Ashabi*   Pages 786 - 801 ( 16 )

Abstract:


AMP-activated protein kinase (AMPK) is a serine/threonine kinase and a driving or deterrent factor in the development of neurodegenerative diseases and dementia. AMPK affects intracellular proteins like the mammalian target of rapamycin (mTOR) Peroxisome proliferator-activated receptor-γ coactivator 1-α (among others) contributes to a wide range of intracellular activities based on its downstream molecules such as energy balancing (ATP synthesis), extracellular inflammation, cell growth, and neuronal cell death (such as apoptosis, necrosis, and necroptosis). Several studies have looked at the dual role of AMPK in neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and Huntington disease (HD) but the exact effect of this enzyme on dementia, stroke, and motor neuron dysfunction disorders has not been elucidated yet. In this article, we review current research on the effects of AMPK on the brain to give an overview of the relationship. More specifically, we review the neuroprotective or neurodegenerative effects of AMPK or AMPK activators like metformin, resveratrol, and 5-aminoimidazole-4-carboxamide- 1-β-d-ribofuranoside on neurological diseases and dementia, which exert through the intracellular molecules involved in neuronal survival or death.

Keywords:

AMPK, dementia, neurodegenerative disease, brain, neuroprotective, AMPK activators.

Affiliation:

Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Department of Neuroscience, University of Florida, College of Medicine and McKnight Brain Institute, Gainesville, FL, 32610, Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran

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