Expanding roles for AMP‐activated protein kinase in neuronal survival and autophagy |
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| Authors: | Jeroen Poels Milo? R Spasi? Patrick Callaerts Koenraad K Norga |
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| Institution: | 1. Laboratory of Developmental Genetics, VIB, Leuven, Belgium;2. Pediatric Hematology and Oncology, Department of Woman and Child, K.U. Leuven, Leuven, Belgium;3. Current address: Laboratory for Membrane Trafficking, Center for Human Genetics (K.U. Leuven) and Department for Molecular and Developmental Genetics (VIB), Leuven, Belgium;4. Laboratory of Developmental Genetics, Department of Human Genetics, K.U. Leuven, Leuven, Belgium |
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| Abstract: | AMP‐activated protein kinase (AMPK) is an evolutionarily conserved cellular switch that activates catabolic pathways and turns off anabolic processes. In this way, AMPK activation can restore the perturbation of cellular energy levels. In physiological situations, AMPK senses energy deficiency (in the form of an increased AMP/ATP ratio), but it is also activated by metabolic insults, such as glucose or oxygen deprivation. Metformin, one of the most widely prescribed anti‐diabetic drugs, exerts its actions by AMPK activation. However, while the functions of AMPK as a metabolic regulator are fairly well understood, its actions in neuronal cells only recently gained attention. This review will discuss newly emerged functions of AMPK in neuroprotection and neurodegeneration. Additionally, recent views on the role of AMPK in autophagy, an important catabolic process that is also involved in neurodegeneration and cancer, will be highlighted. |
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| Keywords: | AMP‐activated protein kinase autophagy metabolism neurodegeneration neuroprotection |
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