Background and activities
Professor Ursula Sonnewald main research interest is in neurochemistry.
At present her research is carried out using a wide range of advanced analytical methods with application to both preclinical and basic research. The main focus of her group is to study glial neuronal interactions in neurodegenerative diseases, especially Alzheimer’s dementia and epilepsy. Our main tools are 13C-and 1H- Magnetic Resonance Spectroscopy, mass spectrometry and HPLC. The low natural abundance of 13C (1.1%) is an advantage in that 13C-enriched precursors can be used for metabolic pathway mapping with little or no background interference from endogenous metabolites. Using animal models of human disease and injection of 13C labeled substrates such as [1-13C]glucose information about metabolic deficiencies can be discovered and new treatment can de designed. She has successfully supervised 19 PhD and 21 master students. Published full scientific papers: 186; citations 2515.
Scientific, academic and artistic work
A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database
- (2015) Glutamate neurotransmission is affected in prenatally stressed offspring. Neurochemistry International. vol. 88.
- (2015) Characterization of glucose-related metabolic pathways in differentiated rat oligodendrocyte lineage cells. Glia.
- (2015) No improvement of neuronal metabolism in the reperfusion phase with melatonin treatment after hypoxic-ischemic brain injury in the neonatal rat. Journal of Neurochemistry.
- (2015) Glucose metabolism and astrocyte-neuron interactions in the neonatal brain. Neurochemistry International. vol. 82.
- (2015) Astrocyte-neuronal interactions in epileptogenesis. Journal of Neuroscience Research. vol. 93 (7).
- (2015) The anticonvulsant actions of carisbamate associate with alterations in astrocyte glutamine metabolism in the lithium-pilocarpine epilepsy model. Journal of Neurochemistry. vol. 132 (5).
- (2015) Modification of Astrocyte Metabolism as an Approach to the Treatment of Epilepsy: Triheptanoin and Acetyl-l-Carnitine. Neurochemical Research.
- (2015) Acetyl-l-carnitine versus placebo for migraine prophylaxis: A randomized, triple-blind, crossover study. Cephalalgia. vol. 35 (11).
- (2015) Glutamate: Where does it come from and where does it go?. Neurochemistry International. vol. 88.
- (2014) The GLT-1 (EAAT2; Slc1a2) glutamate transporter is essential for glutamate homeostasis in the neocortex of the mouse. Journal of Neurochemistry. vol. 128 (5).
- (2014) The pentose phosphate pathway and pyruvate carboxylation after neonatal hypoxic-ischemic brain injury. Journal of Cerebral Blood Flow and Metabolism. vol. 34.
- (2014) Triheptanoin partially restores levels of tricarboxylic acid cycle intermediates in the mouse pilocarpine model of epilepsy. Journal of Neurochemistry. vol. 129 (1).
- (2014) Altered astrocyte-neuronal interactions after hypoxia-ischemia in the neonatal brain in female and male rats. Stroke. vol. 45 (9).
- (2014) Neuron-astrocyte interactions, pyruvate carboxylation and the pentose phosphate pathway in the neonatal rat brain. Neurochemical Research. vol. 39 (3).
- (2014) Early Differences in Dorsal Hippocampal Metabolite Levels in Males But Not Females in a Transgenic Rat Model of Alzheimer's Disease. Neurochemical Research. vol. 39 (2).
- (2014) Neuronal and astrocytic metabolism in a transgenic rat model of Alzheimer's disease. Journal of Cerebral Blood Flow and Metabolism. vol. 34 (5).
- (2014) Glutamate synthesis has to be matched by its degradation - where do all the carbons go?. Journal of Neurochemistry. vol. 131 (4).
- (2014) A subconvulsive dose of kainate selectively compromises astrocytic metabolism in the mouse brain in vivo. Journal of Cerebral Blood Flow and Metabolism. vol. 34 (8).
- (2014) The Glutamine–Glutamate/GABA Cycle: Function, Regional Differences in Glutamate and GABA Production and Effects of Interference with GABA Metabolism. Neurochemical Research. vol. 40 (2).
- (2013) Brain mitochondrial metabolic dysfunction and glutamate level reduction in the pilocarpine model of temporal lobe epilepsy in mice. Journal of Cerebral Blood Flow and Metabolism. vol. 33 (7).