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Alzheimer's disease;; long-term potentiation;; neurodegeneration;; protein;; synthesis;; signaling;; translation;; EUKARYOTIC ELONGATION-FACTOR-2 KINASE;; ALZHEIMERS-DISEASE;; TRANSLATIONAL;; REGULATION;; MEMORY DEFICITS;; ENERGY SENSOR;; LIFE-SPAN;; PHOSPHORYLATION;; MECHANISMS;; PATHWAY;; HOMEOSTASIS;; Neurosciences
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Full-Text Articles in Medicine and Health Sciences
Inhibition Of Amp-Activated Protein Kinase Signaling Alleviates Impairments In Hippocampal Synaptic Plasticity Induced By Amyloid Beta, T. Ma, Y. R. Chen, V. Vingtdeux, H. T. Zhao, B. Viollet, P. Marambaud, E. Klann
Inhibition Of Amp-Activated Protein Kinase Signaling Alleviates Impairments In Hippocampal Synaptic Plasticity Induced By Amyloid Beta, T. Ma, Y. R. Chen, V. Vingtdeux, H. T. Zhao, B. Viollet, P. Marambaud, E. Klann
Journal Articles
The AMP-activated protein kinase (AMPK) is a Ser/Thr kinase that is activated in response to low-energy states to coordinate multiple signaling pathways to maintain cellular energy homeostasis. Dysregulation of AMPK signaling has been observed in Alzheimer's disease (AD), which is associated with abnormal neuronal energy metabolism. In the current study we tested the hypothesis that aberrant AMPK signaling underlies AD-associated synaptic plasticity impairments by using pharmacological and genetic approaches. We found that amyloid beta (A beta)-induced inhibition of long-term potentiation (LTP) and enhancement of long-term depression were corrected by the AMPK inhibitor compound C (CC). Similarly, LTP impairments in APP/PS1 …