High brain lactate is a hallmark of aging and caused by a shift in the lactate dehydrogenase A/B ratio

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 46; pp. 20087 - 20092
• Main Authors: Ross, Jaime M., Öberg, Johanna, Brené, Stefan, Coppotelli, Giuseppe, Terzioglu, Mügen, Pernold, Karin, Goiny, Michel, Sitnikov, Rouslan, Kehr, Jan, Trifunovic, Aleksandra, Larsson, Nils-Göran, Hoffer, Barry J., Olson, Lars, Bloom, Floyd
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 16.11.2010; National Acad Sciences
• Subjects: Aging; Aging - metabolism; Animals; Biological Sciences; Brain; Brain - enzymology; Central nervous system; Cerebral cortex; Dehydrogenases; Deoxyribonucleic acid; DNA; DNA, Mitochondrial - genetics; Electron transport; Enzymes; Gene Expression Regulation, Enzymologic; Genotype & phenotype; High-performance liquid chromatography; Hippocampus; Isoenzymes; Isoenzymes - genetics; Isoenzymes - metabolism; L-Lactate dehydrogenase; L-Lactate Dehydrogenase - genetics; L-Lactate Dehydrogenase - metabolism; Lactates; Lactic acid; Lactic Acid - metabolism; Magnetic resonance spectroscopy; Medicin och hälsovetenskap; Messenger RNA; Metabolism; Mice; Mitochondria; Mitochondria - enzymology; Mitochondria - pathology; Mitochondrial DNA; Mutation; Mutation - genetics; Neurons; Organ Specificity; Premature aging; Proteins; Pyruvic acid; Spectrophotometry; Transcription

At present, there are few means to track symptomatic stages of CNS aging. Thus, although metabolic changes are implicated in mtDNA mutation-driven aging, the manifestations remain unclear. Here, we used normally aging and prematurely aging mtDNA mutator mice to establish a molecular link between mit...