Lipoic acid restores age-associated impairment of brain energy metabolism through the modulation of Akt/JNK signaling and PGC1α transcriptional pathway

Keyphrases

• Transcriptional Pathways 100%
• Age-associated 100%
• Lipoic Acid 100%
• C-Jun N-terminal Kinase Signaling 100%
• PGC-1 100%
• Associated Impairments 100%
• Brain Energy Metabolism 100%
• Glucose Transporter 1 (GLUT1) 66%
• Old Age 66%
• Mitochondrial Biogenesis 66%
• Brain Aging 66%
• Hypometabolic State 66%
• Acid Treatment 33%
• Young Age 33%
• Mitochondria 33%
• F344 Rats 33%
• Multiple Aspects 33%
• Age-related 33%
• Insulin Signaling 33%
• Energy Homeostasis 33%
• Cerebral Glucose Metabolism 33%
• Insulin Sensitivity 33%
• Middle-aged 33%
• PI3K-Akt Pathway 33%
• Microvascular Endothelium 33%
• Glucose Uptake 33%
• Energy Metabolism 33%
• Mitochondrial Bioenergetics 33%
• MicroPET 33%
• GLUT3 33%

Biochemistry, Genetics and Molecular Biology

• N-Terminus 100%
• Kinase 100%
• Phosphotransferase 100%
• Lipoic Acid 100%
• Energy Metabolism 100%
• Glucose Transport 66%
• Mitochondrial Biogenesis 66%
• Mitochondrion 33%
• Downregulation 33%
• Homeostasis 33%
• Glucose Transporter 33%
• Insulin Signaling 33%
• Bioenergy 33%
• Animal Model 33%
• GLUT1 33%
• Fischer 344 Rat 33%
• Glucose Brain Level 33%
• GLUT3 33%

Neuroscience

• Amino Terminal Sequence 100%
• Kinase 100%
• Energy Metabolism 100%
• Lipoic Acid 100%
• Glucose Transport 66%
• Mitochondrial Biogenesis 66%
• Insulin Signaling 33%
• Mitochondrion 33%
• Glucose Transporter 1 33%
• Glucose Transporter 3 33%